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A fundamental goal of developmental biology is to understand how cell and tissue fates are specified. The imaginal discs of Drosophila are excellent model systems for addressing this paradigm as their fate can be redirected when discs regenerate after injury or when key selector genes are misregulated. Here, we show that when Polycomb expression is reduced, the wing selector gene vestigial is ectopically activated. This leads to the inappropriate formation of the Vestigial-Scalloped complex, which forces the eye to transform into a wing. We further demonstrate that disrupting this complex does not simply block wing formation or restore eye development. Instead, immunohistochemistry and high-throughput genomic analysis show that the eye-antennal disc unexpectedly undergoes hyperplastic growth with multiple domains being organized into other imaginal discs and tissues. These findings provide insight into the complex developmental landscape that tissues must navigate before adopting their final fate. [ABSTRACT FROM AUTHOR]

Background: The presence of a human tail is a rare condition resulting from an embryonic remnant that fits the definition of a caudal appendage. It may be a vestigial (true) or a pseudotail. Both may be considered markers of underlying intraspinal abnormalities., Case Description: The present case documents a 5-year-old girl with a caudal appendage in the lumbar region, with a previously normal neurological examination. Spinal magnetic resonance imaging (MRI) showed the presence of occult spinal dysraphism associated with a cutaneous appendage with lipomatous content. We performed microsurgical treatment to excise the lesion and explore the occult spinal dysraphism. A histopathological examination revealed mature adipose tissue with blood vessels and nerve fibers and no bone or cartilage tissue., Conclusion: The presence of a tail-like appendage in the lumbosacral region must alert to the possibility of underlying occult spinal dysraphism. Preoperative assessment must include a complete neurological examination and a detailed MRI evaluation., Competing Interests: There are no conflicts of interest., (Copyright: © 2024 Surgical Neurology International.)

Introduction: The muscles of posterior abdominal wall on each side of vertebral column include psoas group, quadratus lumborum and iliacus. The psoas muscle group comprises of major, minor and tertius. The psoas major is present in all individuals. Psoas minor is often absent in 40% of the cases. Psoas minor muscle has racial and morphometric variations. Aim: To find the incidence and morphology of psoas minor in South Indian population and discuss its clinical implications. Materials and Methods: The present observational cadaveric study was done on 30 embalmed cadavers for teaching purpose from November 2017 to December 2020 at Karnataka Institute of Medical Sciences, Hubballi, Karnataka, India. Cadavers in the study were of the age group between 50-60 years. Out of 30 cadavers, five were females and 25 were males. In cadavers with presence of psoas minor muscle following parameters were photographed and studied: unilateral or bilateral, origin, insertion, nerve supply, total length of musculotendinous unit, length of muscle belly, length of tendon, width and circumference at its widest point. Vernier calipers, measuring tape, scale and inelastic thread were used to note various parameters and were tabulated. Results: Out of 30 cadavers, psoas minor was present in 10 cadavers (two female and eight male), bilateral in five and unilateral in five cadavers. The incidence of presence of psoas minor muscle in the present study is 33.33% (two female 6.67% and eight male 26.67%). Conclusion: The psoas minor muscle being vestigial and inconstant, its morphology is highly variable. But the incidence of psoas minor is quiet significant (33.33%). Hence knowledge of psoas minor is important to anatomists for academic purpose and to clinicians for proper diagnosis and treatment.

RNA interference (RNAi) has developed rapidly as a potential "green" pest management strategy. At present, most studies have focused on the screening of aphid lethal genes, whereas only a few studies have been conducted on wing development, which is crucial for aphid migration and plant‐virus dissemination. Here, the Myzus persicae genes vestigial (vg) and Ultrabithorax (Ubx) related to wing development, were cloned. These two genes were expressed in various tissues of 3rd‐instar winged aphids. The mRNA level of vg was high in 3rd‐instar nymphs, whereas the expression level of Ubx was high in adults. The nanocarrier‐mediated delivery system delivered double‐stranded RNAs for aphid RNAi using topical and root applications. The expression levels of vg and Ubx were downregulated by 44.0% and 36.5%, respectively, using the topical application. The simultaneous RNAi of the two target genes caused 63.3% and 32.2% wing aberration rates using topical and root applications, respectively. The current study provided a promising method for controlling aphid migration to alleviate the spread of insect transmitted plant diseases. [ABSTRACT FROM AUTHOR]

The evolution and variations of human anatomy are of great interest to physicians and anatomists. Variations can be categorized as vestigial, accessory or atavistic structures. Vestigial muscles are frequently encountered structures that are normally present but have become rudimentary through evolution. Muscles that disappeared during evolution sometimes arise again, although rarely; such muscles are referred to as atavistic. They arise from failure of suppression of genetic loci. Some common atavistic muscles seen clinically are the extensor digitorum brevis manus, chondroepitrochlearis and plantaris. Atavistic muscles appear more frequently in the upper limb than in any other region of the human body. One explanation for the appearance of these muscles, mainly within the upper limbs, is based on the evolution of the complex upper extremities formed in humans today. Often, the presence of atavistic muscles is asymptomatic, but they can compromise the function of normal anatomical structures and complicate clinical situations if their presence is unknown. They can cause complications if they are confused with soft tissue pathology, if they compress or displace surrounding structures, or if they require an additional blood supply during times of exercise and stress. The purpose of this paper was to describe the common atavistic muscles, their hypothesized evolutionary origins, their potential complications and possible treatments for the diagnosing clinician. [ABSTRACT FROM AUTHOR]

The mammalian dentition is a serially homogeneous structure that exhibits wide numerical and morphological variation among multiple different species. Patterning of the dentition is achieved through complex reiterative molecular signaling interactions that occur throughout the process of odontogenesis. The secreted signaling molecule Sonic hedgehog (Shh) plays a key role in this process, and the Shh coreceptor growth arrest-specific 1 (Gas1) is expressed in odontogenic mesenchyme and epithelium during multiple stages of tooth development. We show that mice engineered with Gas1 loss-of-function mutation have variation in number, morphology, and size of teeth within their molar dentition. Specifically, supernumerary teeth with variable morphology are present mesial to the first molar with high penetrance, while molar teeth are characterized by the presence of both additional and absent cusps, combined with reduced dimensions and exacerbated by the presence of a supernumerary tooth. We demonstrate that the supernumerary tooth in Gas1 mutant mice arises through proliferation and survival of vestigial tooth germs and that Gas1 function in cranial neural crest cells is essential for the regulation of tooth number, acting to restrict Wnt and downstream FGF signaling in odontogenic epithelium through facilitation of Shh signal transduction. Moreover, regulation of tooth number is independent of the additional Hedgehog coreceptors Cdon and Boc, which are also expressed in multiple regions of the developing tooth germ. Interestingly, further reduction of Hedgehog pathway activity in Shh tm6Amc hypomorphic mice leads to fusion of the molar field and reduced prevalence of supernumerary teeth in a Gas1 mutant background. Finally, we demonstrate defective coronal morphology and reduced coronal dimensions in the molar dentition of human subjects identified with pathogenic mutations in GAS1 and SHH/GAS1, suggesting that regulation of Hedgehog signaling through GAS1 is also essential for normal patterning of the human dentition. [ABSTRACT FROM AUTHOR]

The vertebrate limb is a dynamic structure which has evolved into many diverse forms to facilitate complex behavioral adaptations. The principle molecular and cellular processes that underlie development of the vertebrate limb are well characterized. However, how these processes are altered to drive differential limb development between vertebrates is less well understood. Several vertebrate models are being utilized to determine the developmental basis of differential limb morphogenesis, though these typically focus on later patterning of the established limb bud and may not represent the complete developmental trajectory. Particularly, heterochronic limb development can occur prior to limb outgrowth and patterning but receives little attention. This review summarizes the genetic regulation of vertebrate forelimb diversity, with particular focus on wing reduction in the flightless emu as a model for examining limb heterochrony. These studies highlight that wing reduction is complex, with heterochronic cellular and genetic events influencing the major stages of limb development. Together, these studies provide a broader picture of how different limb morphologies may be established during development. Key Findings: Limb development progresses through several stages induced by key molecular regulators.Limb evolution can occur through changes to one of many of these processes.However little attention has focused on the early stages of limb field specification.The flightless emu possesses a vestigial wing and is an excellent model to examine differential limb development.Emu wing heterochrony is complex and occurs through altered molecular regulation across several stages of limb development. [ABSTRACT FROM AUTHOR]

Abstract Background Most aphids exhibit wing polyphenism in which wingless and winged morphs produce depending on the population density and host plant quality. Although the influence of environmental factors on wing polyphenism of aphids have been extensively investigated, molecular mechanisms underlining morph differentiation (i.e. wing development /degeneration), one downstream aspect of the wing polyphenism, has been poorly understood. Results We examined the expression levels of the twenty genes involved in wing development network, and only vestigial (vg) showed significantly different expression levels in both whole-body and wall-body of third instar nymphs, with 5.4- and 16.14- fold higher expression in winged lines compared to wingless lines, respectively in Rhopalosiphum padi. vg expression was higher in winged lines compared to wingless lines in third, fourth instar nymphs and adults. Larger difference expression was observed in third (21.38-fold) and fourth (20.91-fold) instar nymphs relative to adults (3.12-fold). Suppression of vg using RNAi repressed the wing development of third winged morphs. Furthermore, dual luciferase reporter assay revealed that the miR-147 can target the vg mRNA. Modulation of miR-147b levels by microinjection of its agomir (mimic) decreased vg expression levels and repressed wing development. Conclusions Our findings suggest that vg is essential for wing development in R. padi and that miR-147b modulates its expression.

The acquisition of wings has facilitated the massive evolutionary success of pterygotes (winged insects), which now make up nearly three‐quarters of described metazoans. However, our understanding of how this crucial structure has evolved remains quite elusive. Historically, two ideas have dominated in the wing origin debate, one placing the origin in the dorsal body wall (tergum) and the other in the lateral pleural plates and the branching structures associated with these plates. Through studying wing‐related tissues in the wingless segments (such as wing serial homologs) of the beetle, Tribolium castaneum, we obtained several crucial pieces of evidence that support a third idea, the dual origin hypothesis, which proposes that wings evolved from a combination of tergal and pleural tissues. Here, we extended our analysis outside of the beetle lineage and sought to identify wing‐related tissues from the wingless segments of the cockroach, Blattella germanica. Through detailed functional and expression analyses for a critical wing gene, vestigial (vg), along with re‐evaluating the homeotic transformation of a wingless segment induced by an improved RNA interference protocol, we demonstrate that B. germanica possesses two distinct tissues in their wingless segments, one with tergal and one with pleural nature, that might be evolutionarily related to wings. This outcome appears to parallel the reports from other insects, which may further support a dual origin of insect wings. However, we also identified a vg‐independent tissue that contributes to wing formation upon homeotic transformation, as well as vg‐dependent tissues that do not appear to participate in wing formation, in B. germanica, indicating a more complex evolutionary history of the tissues that contributed to the emergence of insect wings. Research Highlights: Diverse types of wing‐related tissues identified in cockroaches provide new insight into the complex evolutionary history of the tissues that contributed to the emergence of insect wings, a chief example of morphological novelty. [ABSTRACT FROM AUTHOR]

Vestigial-like family (VGLL) members are mammalian orthologs of vestigial gene in Drosophila, and they consist of four homologs (VGLL1–4). VGLL members have TDU motifs that are binding regions to TEA/ATSS-DNA-binding domain transcription factor (TEAD). Through TDU motifs, VGLL members act as transcriptional cofactors for TEAD. VGLL1-3 have single TDU motif, whereas VGLL4 has two tandem TDU motifs, suggesting that VGLL4 has distinct molecular functions among this family. Although molecular and physiological functions of VGLL members are still obscure, emerging evidence has shown that these members are involved in tumor development. Gene alterations and elevated expression of VGLL1-3 were observed in various types of tumors, and VGLL1-3 have been shown to possess tumorigenic functions. In contrast, down-regulation of VGLL4 was detected in various tumors, and the tumor-suppressing role of VGLL4 has been demonstrated. In this review, we summarize the recently identified multiple roles of VGLL members in tumor development and provide important and novel insights regarding tumorigenesis.

The Decapentaplegic (Dpp) and Wingless (Wg) signal pathways play important roles in numerous biological processes in Drosophila. The Drosophila vestigial (vg) gene is selectively required for wing imaginal disc cell proliferation, which is essential for the formation of the adult wing and halter structures, and is regulated by Dpp and Wg signaling. Using a Drosophila invasion model of wing epithelium, we showed herein that inhibition of Dpp or Wg signaling promoted cells to migrate across the cell lineage restrictive anterior/posterior (A/P) compartment boundary. Being downstream of both Dpp and Wg signaling, vg can block cell migration induced by loss of either pathway. In addition, suppression of vg is sufficient to induce cell migration across the A/P boundary. Transcriptomic analysis revealed potential downstream genes involved in the cell migration after suppressing vg in the wing disc. We further demonstrated that the c‐Jun N‐terminal kinase (JNK) signaling promoted cell migration induced by vg suppression by upregulating Caspase activity. Taken together, our results revealed the requirement of Vg for suppressing cell migration and clarified how developmental signals collaborate to stabilize cells along the compartment boundary. [ABSTRACT FROM AUTHOR]

Changes in the effect of methotrexate (400 μg/kg nutrient medium) combined with high temperature (28°C) of ontogenesis were studied on two hybrid lines of Drosophila melanogaster heterozygous by the vestigial gene that underwent long-term target selection for cutting injury of the wing. Changes in the wing shape, mortality rate, and morphology of polytene chromosomes were studied. [ABSTRACT FROM AUTHOR]

Organs mainly attain their size by cell growth and proliferation, but sometimes also grow through recruitment of undifferentiated cells. Here we investigate the participation of cell recruitment in establishing the pattern of Vestigial (Vg), the product of the wing selector gene in Drosophila. We find that the Vg pattern overscales along the dorsal-ventral (DV) axis of the wing imaginal disc, i.e., it expands faster than the DV length of the pouch. The overscaling of the Vg pattern cannot be explained by differential proliferation, apoptosis, or oriented-cell divisions, but can be recapitulated by a mathematical model that explicitly considers cell recruitment. When impairing cell recruitment genetically, we find that the Vg pattern almost perfectly scales and adult wings are approximately 20% smaller. Conversely, impairing cell proliferation results in very small wings, suggesting that cell recruitment and cell proliferation additively contribute to organ growth in this system. Furthermore, using fluorescent reporter tools, we provide direct evidence that cell recruitment is initiated between early and mid third-instar larval development. Altogether, our work quantitatively shows when, how, and by how much cell recruitment shapes the Vg pattern and drives growth of the Drosophila wing. Image 1 • In the Drosophila wing, the pattern of Vestigial overscales relative to tissue size. • The overscaling of the Vestigial pattern is driven by a cell recruitment mechanism. • Using the TransTimer reporters, cell recruitment is observed in wild-type discs. • Cell recruitment contributes to about 20% of the Drosophila wing. • Cell proliferation and recruitment contribute additively to adult wing size. [ABSTRACT FROM AUTHOR]

Background: Most aphids exhibit wing polyphenism in which wingless and winged morphs produce depending on the population density and host plant quality. Although the influence of environmental factors on wing polyphenism of aphids have been extensively investigated, molecular mechanisms underlining morph differentiation (i.e. wing development /degeneration), one downstream aspect of the wing polyphenism, has been poorly understood. Results: We examined the expression levels of the twenty genes involved in wing development network, and only vestigial (vg) showed significantly different expression levels in both whole-body and wall-body of third instar nymphs, with 5.4- and 16.14- fold higher expression in winged lines compared to wingless lines, respectively in Rhopalosiphum padi. vg expression was higher in winged lines compared to wingless lines in third, fourth instar nymphs and adults. Larger difference expression was observed in third (21.38-fold) and fourth (20.91-fold) instar nymphs relative to adults (3.12-fold). Suppression of vg using RNAi repressed the wing development of third winged morphs. Furthermore, dual luciferase reporter assay revealed that the miR-147 can target the vg mRNA. Modulation of miR-147b levels by microinjection of its agomir (mimic) decreased vg expression levels and repressed wing development. Conclusions: Our findings suggest that vg is essential for wing development in R. padi and that miR-147b modulates its expression. [ABSTRACT FROM AUTHOR]

Palmaris longus is classified as a phylogenetically retrogressive muscle having a short belly with a long tendon. It varies in the incidence of its absence, form, attachment, duplication and its ability of having accessory slips and substitute structures. The muscle is of interest to hand surgeons because a number of cases have been reported with complaints of a volar distal forearm swelling and median nerve compression symptoms. Therefore, the present study was performed with the purpose to determine the morphology and the variations of PL in North Indian population. Material for the present study consisted of 62 limbs(20 Male and 11 Female) which were made available through a series of dissections performed for first year medical students at SGRDIMSAR, Amritsar, Punjab. The morphology and variations of PL and its relation with neighbouring structures were noted. The data thus collected was stored and compared to other studies. Of 62 limbs dissected 55(88.70%) showed normal morphology of palmaris longus muscle as per the standard textbook. 5 limbs(8.06%) showed complete agenesis. 1(1.61%) limb exhibited a fleshy fusiform PLM. A Reversed palmaris longus muscle(RPLM) along with accessory PL(1.61%) was observed in the same limb. Variations of the PL tendon may even confuse an experienced surgeon. Thus, it is important for the reconstructive surgeons or radiologists to be aware of the possibility of variations and its impact on the structures present at the wrist area especially one that might contribute to median or ulnar nerve compression. [ABSTRACT FROM AUTHOR]

The degree to which molecular and morphological loss of function occurs synchronously during the vestigialization of traits is not well understood. The mammalian vomeronasal system, a sense critical for mediating many social and reproductive behaviors, is highly conserved across mammals. New World Leaf-nosed bats (Phyllostomidae) are under strong selection to maintain a functional vomeronasal system such that most phyllostomids possess a distinct vomeronasal organ and an intact TRPC2, a gene encoding a protein primarily involved in vomeronasal sensory neuron signal transduction. Recent genetic evidence, however, shows that TRPC2 is a pseudogene in some Caribbean nectarivorous phyllostomids. The loss-of-function mutations suggest the sensory neural tissue of the vomeronasal organ is absent in these species despite strong selection on this gene in its mainland relatives, but the anatomy was unknown in most Caribbean nectarivorous phyllostomids until this study. We used diffusible iodine-based contrast-enhanced computed tomography (diceCT) to test whether the vomeronasal and main olfactory anatomy of several phyllostomid species matched genetic evidence of function, providing insight into whether loss of a structure is linked to pseudogenization of a molecular component of the system. The vomeronasal organ is indeed rudimentary or absent in species with a disrupted TRPC2 gene. Caribbean nectar-feeders also exhibit derived olfactory turbinal morphology and a large olfactory recess that differs from closely related bats that have an intact vomeronasal organ, which may hint that the main olfactory system may compensate for loss. We emphasize non-invasive diceCT is capable of detecting the vomeronasal organ, providing a feasible approach for quantifying mammalian chemosensory anatomy across species.

The degree to which molecular and morphological loss of function occurs synchronously during the vestigialization of traits is not well understood. The mammalian vomeronasal system, a sense critical for mediating many social and reproductive behaviors, is highly conserved across mammals. New World Leaf-nosed bats (Phyllostomidae) are under strong selection to maintain a functional vomeronasal system such that most phyllostomids possess a distinct vomeronasal organ and an intact TRPC2, a gene encoding a protein primarily involved in vomeronasal sensory neuron signal transduction. Recent genetic evidence, however, shows that TRPC2 is a pseudogene in some Caribbean nectarivorous phyllostomids. The loss-of-function mutations suggest the sensory neural tissue of the vomeronasal organ is absent in these species despite strong selection on this gene in its mainland relatives, but the anatomy was unknown in most Caribbean nectarivorous phyllostomids until this study. We used diffusible iodine-based contrast-enhanced computed tomography (diceCT) to test whether the vomeronasal and main olfactory anatomy of several phyllostomid species matched genetic evidence of function, providing insight into whether loss of a structure is linked to pseudogenization of a molecular component of the system. The vomeronasal organ is indeed rudimentary or absent in species with a disrupted TRPC2 gene. Caribbean nectar-feeders also exhibit derived olfactory turbinal morphology and a large olfactory recess that differs from closely related bats that have an intact vomeronasal organ, which may hint that the main olfactory system may compensate for loss. We emphasize non-invasive diceCT is capable of detecting the vomeronasal organ, providing a feasible approach for quantifying mammalian chemosensory anatomy across species. [ABSTRACT FROM AUTHOR]

With the recent finding that the vestigial-like family member 3 ( Vgll3 ) gene is associated with early maturation, we decided to re-examine previously reported quantitative trait loci (QTL) and genome wide association (GWA) studies, involved with early maturation, to see if Vgll3 was the source of any of these associations. Using a TaqMan assay for Vgll3 , we were able to verify that a prominent QTL for early maturation was indeed associated with Vgll3 . Next, we used Vgll3 genotypes as a cofactor to re-examine for any additional QTLs or GWAs. Several were found at the chromosome-wide significance level. By examining interacting partners of Vgll3 from other organisms, we identified several candidate genes that may interact with Vgll3 in Atlantic salmon and effect early maturation. The location of these genes were determined from the genome sequence, while markers near QTL were examined to see if they were near any Vgll3 interacting genes. In this way, we identified TEAD3 as a putative gene also influencing early maturation in Atlantic salmon. A TaqMan assay was used to genotype TEAD3 . These genotypes appear to be associated with early maturation. [ABSTRACT FROM AUTHOR]

The Drosophila vestigial gene is required for proliferation and differentiation of the adult wing and for differentiation of larval and adult muscle identity. Vestigial is part of a multi-protein transcription factor complex, which includes Scalloped, a TEAD-class DNA binding protein. Binding Scalloped is necessary for translocation of Vestigial into the nucleus. We show that Vestigial is extensively post-translationally modified and at least one of these modifications is required for proper function during development. We have shown that there is p38-dependent phosphorylation of Serine 215 in the carboxyl-terminal region of Vestigial. Phosphorylation of Serine 215 occurs in the nucleus and requires the presence of Scalloped. Comparison of a phosphomimetic and non-phosphorylatable mutant forms of Vestigial shows differences in the ability to rescue the wing and muscle phenotypes associated with a null vestigial allele. [ABSTRACT FROM AUTHOR]

True human tails are rare vestigial structures that are typically removed in childhood. Here a case is presented in which an inconspicuous sacrococcygeal tail was incidentally discovered in late adulthood. A 56-year-old man with no significant past medical history presented to a dermatology clinic with a chief complaint of a hyperpigmented lesion on his central back. However, on full body skin exam, a separate flesh-colored 0.7 cm × 0.5 cm appendage was discovered in the midline sacrococcygeal region. This lesion had been present and unchanged since childhood. This particular lesion was removed via shave biopsy. Microscopic exam found it to be consistent with a diagnosis of a true human tail. There were no apparent involved spinal cord structures, and no further treatment was thought to be necessary. Human tails are congenital anomalies associated with occult spinal lesions in about 50% of cases. Therefore, it is in these patients' best interest to thoroughly evaluate for spinal cord involvement prior to biopsy. There is a relative lack of literature published on the topic, and a greater awareness of human tails would be helpful to ensure their inclusion in a differential diagnosis for persistent sacrococcygeal lesions in patients of any age. [ABSTRACT FROM AUTHOR]

The members of the vestigial-like gene family have been identified as homologs of the Drosophila vestigial, which is essential to wing formation. All members of the family are characterized by the presence of the TONDU domain, a highly conserved sequence that mediates their interaction with the transcription factors of the TEAD family. Mammals possess four vestigial-like genes that can be subdivided into two classes, depending on the number of Tondu domains present. While vestigial proteins have been studied in great depth in Drosophila, we still have sketchy knowledge of the functions of vestigial-like proteins in vertebrates. Recent studies have unveiled unexpected functions for some of these members and reveal the role they play in the Hippo pathway. Here, we present the current knowledge about vestigial-like family gene members and their functions, together with their identification in different taxa. [ABSTRACT FROM AUTHOR]

Scaling between specific organs and overall body size has long fascinated biologists, being a primary mechanism by which organ shapes evolve. Yet, the genetic mechanisms that underlie the evolution of scaling relationships remain elusive. Here, we compared wing and fore tibia lengths (the latter as a proxy of body size) in Drosophila melanogaster, Drosophila simulans, Drosophila ananassae and Drosophila virilis, and show that the first three of these species have roughly a similar wing-to-tibia scaling behavior. In contrast, D. virilis exhibits much smaller wings relative to their body size compared with the other species and this is reflected in the intercept of the wing-to-tibia allometry. We then asked whether the evolution of this relationship could be explained by changes in a specific cis-regulatory region or enhancer that drives expression of the wing selector gene, vestigial (vg), whose function is broadly conserved in insects and contributes to wing size. To test this hypothesis directly, we used CRISPR/Cas9 to replace the DNA sequence of the predicted Quadrant Enhancer (vgQE) from D. virilis for the corresponding vgQE sequence in the genome of D. melanogaster. Strikingly, we discovered that D. melanogaster flies carrying the D. virilis vgQE sequence have wings that are significantly smaller with respect to controls, partially shifting the intercept of the wing-to-tibia scaling relationship towards that observed in D. virilis. We conclude that a single cis-regulatory element in D. virilis contributes to constraining wing size in this species, supporting the hypothesis that scaling could evolve through genetic variations in cis-regulatory elements., Competing Interests: Competing interests The authors declare no competing or financial interests., (© 2023. Published by The Company of Biologists Ltd.)

Winged insects underwent an unparalleled evolutionary radiation, but mechanisms underlying the origin and diversification of wings in basal insects are sparsely known compared with more derived holometabolous insects. In the neopteran species Oncopeltus fasciatus, we manipulated wing specification genes and used RNA-seq to obtain both functional and genomic perspectives. Combined with previous studies, our results suggest the following key steps in wing origin and diversification. First, a set of dorsally derived outgrowths evolved along a number of body segments including the first thoracic segment (T1). Homeotic genes were subsequently co-opted to suppress growth of some dorsal flaps in the thorax and abdomen. In T1 this suppression was accomplished by Sex combs reduced, that when experimentally removed, results in an ectopic T1 flap similar to prothoracic winglets present in fossil hemipteroids and other early insects. Global geneexpression differences in ectopic T1 vs. T2/T3 wings suggest that the transition from flaps to wings required ventrally originating cells, homologous with those in ancestral arthropod gill flaps/epipods, to migrate dorsally and fuse with the dorsal flap tissue thereby bringing new functional gene networks; these presumably enabled the T2/T3 wing's increased size and functionality. Third, "fused" wings became both the wing blade and surrounding regions of the dorsal thorax cuticle, providing tissue for subsequent modifications including wing folding and the fit of folded wings. Finally, Ultrabithorax was co-opted to uncouple the morphology of T2 and T3 wings and to act as a general modifier of hindwings, which in turn governed the subsequent diversification of lineage-specific wing forms. [ABSTRACT FROM AUTHOR]

Background: The scalloped ( sd) and vestigial ( vg) genes function together in Drosophila wing development. Little is known about sd protein (SD) expression during development, or whether sd and vg interact in other developing tissues. To begin to address these questions, we generated an anti-SD antibody. Results: During embryogenesis, SD is expressed in both central and peripheral nervous systems, and the musculature. SD is also expressed in developing flight appendages. Despite SD expression herein, the peripheral nervous system, musculature, and dorsal limb primordia appeared generally normal in the absence of sd function. SD is also expressed in subsets of ventral nerve cord cells, including neuroblast 1-2 descendants and ventral unpaired median motor neurons (mVUMs). While sd function is not required to specify these neurons, it is necessary for the correct innervation of somatic muscles by the mVUMs. We also show that SD and vg protein (VG) are co-expressed in overlapping and distinctive subsets of cells in embryonic and larval tissues. Conclusions: We describe the full breadth of SD expression during Drosophila embryogenesis, and identify a requirement for sd function in a subset of motor neurons. This work provides the necessary foundation for functional studies regarding the roles of sd during Drosophila development. Developmental Dynamics 242:874-885, 2013. © 2013 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Abstract: The vestigial (Vg) mutant is a Z-linked mutant that causes vestigial wings in the silkworm, Bombyx mori. We have previously reported a 1.5-Mb interstitial deletion on the Z chromosome bearing the Vg mutation (Z Vg chromosome). In this study, we found that exons 3–8 of a gene named Bmptp-Z encoding a putative tyrosine-specific protein phosphatase are deleted by the 1.5-Mb interstitial deletion. We found that a gene encoding the Bombyx homolog of Drosophila Apterous (BmAp-A) protein is located 4.5 kb downstream of the distal breakpoint of the 1.5-Mb interstitial deletion. Moreover, an in-frame fusion transcript composed of the 5′ part of Bmptp-Z and the 3′ part of Bmap-A is generated specific to the ZVg chromosome. Effects of the in-frame fusion transcript on the vestigial phenotype are discussed. [Copyright &y& Elsevier]

Selector proteins are transcription factors that coordinate the formation and identity of organs and appendages. The proper formation of these tissues requires the selector proteins to regulate the expression of a large set of genes. Many selector proteins are involved in regulating multiple developmental processes, yet it is not completely clear how they are able to activate different sets of genes in a tissue-specific manner. An association with cofactors is thought to be one method by which enhancer selectivity is achieved. During wing development the selector protein Scalloped (SD) interacts with the cofactor Vestigial (VG). This interaction leads to the activation of a specific set of downstream wing genes. Herein, data are presented indicating that the switch in binding selectivity is likely achieved by VG altering the general affinity that the SD protein has for DNA. The decreased affinity for DNA is compensated for by the fact that the VG protein forms a complex containing two SD proteins. These two properties ensure that the SD-VG complex is able to bind only to enhancers that have two consecutive binding sites. Furthermore, data are presented that indicate that the function of the two terminal domains of the VG protein is not restricted to activating transcription and promoting the recruitment of two SD proteins. [ABSTRACT FROM AUTHOR]

In Drosophila melanogaster, Vestigial (Vg) and Scalloped (Sd) form a transcription factor complex and play a crucial role in wing development. To extend our knowledge of insect wing formation, we isolated vg and sd homologues from two ladybird beetle species, Henosepilachna vigintioctopunctata and Harmonia axyridis. Although the ladybird beetle vg homologues had only low homology with D. melanogaster vg, ectopic expression of H. vigintioctopunctata vg induced wing-like tissues in antennae and legs of D. melanogaster. Subsequent larval RNA interference (RNAi) analysis in H. vigintioctopunctata demonstrated conserved functions of vg and sd in wing development, and an unexpected novel function of sd in pupal ecdysis. Furthermore, our results can be applied to the production of a flightless ladybird beetle for biological control purposes using larval RNAi. [ABSTRACT FROM AUTHOR]

Abstract: The control of cell morphology is important for shaping animals during development. Here we address the role of the Wnt/Wingless signal transduction pathway and two of its target genes, vestigial and shotgun (encoding E-cadherin), in controlling the columnar shape of Drosophila wing disc cells. We show that clones of cells mutant for arrow (encoding an essential component of the Wingless signal transduction pathway), vestigial or shotgun undergo profound cell shape changes and are extruded towards the basal side of the epithelium. Compartment-wide expression of a dominant-negative form of the Wingless transducer T-cell factor (TCF/Pangolin), or double-stranded RNA targeting vestigial or shotgun, leads to abnormally short cells throughout this region, indicating that these genes act cell autonomously to maintain normal columnar cell shape. Conversely, overexpression of Wingless, a constitutively-active form of the Wingless transducer β-catenin/Armadillo, or Vestigial, results in precocious cell elongation. Co-expression of Vestigial partially suppresses the abnormal cell shape induced by dominant-negative TCF. We conclude that Wingless signal transduction plays a cell-autonomous role in promoting and maintaining the columnar shape of wing disc cells. Furthermore, our data suggest that Wingless controls cell shape, in part, through maintaining vestigial expression. [Copyright &y& Elsevier]

Abstract: The gene vestigial (vg) plays a key role in indirect flight muscle (IFM) development. We show here that vg is controlled by the Notch anti-myogenic signaling pathway in myoblasts and is regulated by a novel 822 bp enhancer during IFM differentiation. Interestingly, this muscle enhancer is activated in developing fibers and in a small number of myoblasts before the fusion of myoblasts with the developing muscle fibers. Moreover, we show that this enhancer is activated by Drosophila Myocyte enhancing factor 2 (MEF2), Scalloped (SD) and VG but repressed by Twist, demonstrating a sensitivity to differentiation in vivo. In vitro experiments reveal that SD can directly bind this enhancer and MEF2 can physically interact with both SD and TWI. Cumulatively, our data reveal the interplay between different myogenic factors responsible for the expression of an enhancer activated during muscle differentiation. [Copyright &y& Elsevier]

The circadian clock of Drosophila (fruit fly) has been extensively studied as a model system in molecular chronobiology. In Drosophila melanogaster, several clock genes are necessary for the generation and regulation of overt rhythms. Among these, vrille (vri) is a clock gene as well as a clock-controlled gene and its oscillation is essential for circadian rhythms at both molecular and behavioral levels. In this study, we have investigated the rhythmic expression patterns of vri at six time points (ZT 02, ZT 06, ZT 10, ZT 14, ZT 18 and ZT 22) over the 24 h period in peripheral tissues such as intestine and salivary glands of wild type (WT) and mutants [vestigial (vg) and cryptochrome absent (cryb)] of D. melanogaster under LD (12:12) condition. At ZT 14, vri expression was most pronounced in WT and mutants in both tissues compared to other time points. At ZT 22 and ZT 02, the expression was almost nil in both tissues. A definite temporal pattern in the levels of vri expression was observed at ZT 06, ZT 10 and ZT 18 in both tissues (of WT and other mutants). vg flies have greatly reduced wings, their gross locomotor activity was poorer and levels of its expression were also lower than WT flies. In cryb mutant, vri expression was less intensive than WT and vg mutants; this indicates that photic transduction to central/peripheral clock(s) is defective in cryb flies compared to other two types. In this study, we observed the presence of circadian expression patterns of vri in the peripheral oscillators during the developmental stages of Drosophila melanogaster. [ABSTRACT FROM AUTHOR]

It is a well known fact that light is the major environmental cue for the expression of overt circadian rhythms in a wide variety of living organisms including Drosophila. In this study, we have analyzed the period length (τ), amount of activity (α) and phase angle difference (ψ) in wild type, vestigial (vg) and cryb mutants (synthesizing functionless cryptochrome) of Drosophila under different light regime treated (12:12 - white light:dark (LD), blue (450 nm):dark (BD), green (550 nm):dark and red (650 nm):dark (RD)) conditions. Under red light (RD 12:12), period length, amount of activity and phase angle difference were significantly decreased in wild type and mutants, indicating that red light could be less effective on the expression of locomotor rhythms. Further, under blue (BD 12:12) and green (GD 12:12) light, the amount of activity was significantly decreased in vg and cryb mutants than wild type; period length, phase angle difference were significantly decreased in cryb mutants, in blue light, raising the possibility that blue light could mimic darkness in cryb mutants of Drosophila. [ABSTRACT FROM AUTHOR]

In many taxa, females signal during courtship when they are receptive. However, just because a female signals does not mean that the male responds to the signal. This study examines female signaling of receptivity (readiness to copulate) and male response in the parasitoid wasp Spalangia endius Walker. Females folded their antennae against their heads when they were receptive, and antennal folding has been shown to be effective in eliciting male copulation attempts in a confamilial. However, male S. endius did not respond to antennal folding: males did not contact the female's antennae during courtship, and how quickly a male attempted copulation was independent of whether or not the female had antennae. Males courted from on top of the female's abdomen and appeared to detect receptivity directly from the female's abdomen rising as her genital orifice opened. On females whose abdomens did not rise, initiation of male copulation attempts were delayed but not eliminated. Based on its current lack of function as a receptivity signal and on comparisons to published reports of mating behavior in confamilials, we hypothesize that female antennal folding at receptivity is a vestigial trait in S. endius. [ABSTRACT FROM AUTHOR]

Abstract: The vestigial gene has been shown to control skeletal muscle formation in Drosophila and the related Vestigial-like 2 (Vgl-2) protein plays a similar role in mice. Vgl-family proteins are thought to regulate tissue-specific gene expression by binding to members of the broadly expressed Scalloped/Tef/TEAD transcription factor family. Zebrafish have at least four Vgl genes, including two Vgl-2s, and at least three TEAD genes, including two Tead3s. We describe the cloning and expression of one member from each family in the zebrafish. A novel gene, vgl-2b, with closest homology to mouse and human vgl-2, is expressed transiently in nascent notochord and in muscle fibres as they undergo terminal differentiation during somitogenesis. Muscle cells also express a TEAD-3 homologue, a possible partner of Vgl-2b, during myoblast differentiation and early fibre assembly. Tead-3a is also expressed in rhombomeres, eye and epiphysis regions. [Copyright &y& Elsevier]

It has long been noted that high temperature produces great variation in wing forms of the vestigial mutant of Drosophila. Most of the wings have defects in the wing blade and partially formed wing margin, which are the result of autonomous cell death in the presumptive wing blade or costal region of the wing disc. The vestigial gene (vg) and the interaction of Vg protein with other gene products are well understood. With this biochemical knowledge, reinvestigations of the high-temperature-induced vestigial wings and the elucidation of the molecular mechanism underlying the large-scale variation of the wing forms may provide insight into further understanding of development of the wing of Drosophila. As a first step of such explorations, I examined high-temperature-induced (29°C) vestigial wings. In the first part of this paper, I provide evidences to show that the proximal and distal costae in these wings exhibit regular and continuous variation, which suggests different developmental processes for the proximal and distal costal sections. Judging by the costae presenting in the anterior wing margin, I propose that the proximal and distal costal sections are independent growth units. The genes that regulate formation of the distal costal section also strongly affect proliferation of cells nearby; however, the same phenomenon has not been found in the proximal costal section. The distal costal section seems to be an extension of the radius vein. vestigial, one of the most intensely researched temperature-sensitive mutations, is a good candidate for the study of marginal vein formation. In the second part of the paper, I regroup the wing forms of these wings, chiefly by comparison of venation among these wings, and try to elucidate the variation of the wing forms according to the results of previous work and the conclusions reached in the first part of this paper, and provide clues for further researches. [ABSTRACT FROM AUTHOR]

Transposable P elements have been used extensively for Drosophila mutagenesis. While their mutagenic activity has long been recognized, the mechanisms by which P elements cause mutations are varied and not completely understood. We describe here an experiment to replace a P element at vestigial (vg) that caused a strong mutant phenotype (P[21-3]) with a P element (P[21]) known to produce a very weak phenotype when inserted at vg. In addition to testing the feasibility of P element replacements at vg, our investigation led to the production of 7 new vg alleles and 1 apparent second site suppressor. All the vg21-3 revertants that we recovered had a P element inserted into the first exon of vg at the same location and in the same orientation as the original element in vg21-3, providing a unique opportunity to study the mechanism of transposon mutagenesis. A majority of the revertants arose from a previously described event: internal deletion of P sequences, including the P promoter. In addition, 3 novel reversions of the vg21-3 wing phenotype were recovered. The wings of homozygous vg21r36 flies were normal. However, vg21r36 in combination with a deletion of the vg locus exhibited a strong mutant wing phenotype. This was surprising, because the P element insertion in vg21r36 was very similar to that found in the vg21 allele, which showed only slight nicking of the wings in combination with a deletion. In vg21r4, reversion was caused by a tandem insertion of P[21] and the original P[21-3] element present in vg21-3. Finally, the vg21r7 revertant had a P[21-3] insert at vg and 3 additional P elements elsewhere in the genome. We hypothesize that reversion in the 3 novel cases might be caused by P repressor produced by an element at vg or, in the case of vg21r7, elsewhere in the genome. This raises an interesting aspect of P element evolution. While P transposons produce mutations that might prove deleterious to their host, their success in invading the genome of D. melanogaster may be explained by their ability to silence those same mutations by a range of repressor-producing elements. [ABSTRACT FROM AUTHOR]

Abstract: Drosophila dorsal longitudinal muscles develop during metamorphosis by fusion of myoblasts with larval templates. It has been shown that both vestigial and Notch are crucial for correct formation of these muscles. We investigated the relationship between vestigial and the Notch pathway during this process. Using Enhancer of Split Region Transcript m6 gene expression as a reporter of Notch pathway activity, we were able to demonstrate that this pathway is only active in myoblasts. Moreover, close examination of the cellular location of several of the main actors of the N pathway (Notch, Delta, neuralized, Serrate, Mind bomb1 and fringe) during dorsal longitudinal muscle development enabled us to find that Notch receptor can play multiple roles in adult myogenesis. We report that the locations of the two Notch ligands (Delta and Serrate) are different. Interestingly, we found that fringe, which encodes a glycosyltransferase that modifies the affinity of the Notch receptor for its ligands, is expressed in muscle fibers and in a subset of myoblasts. In addition, we demonstrate that fringe expression is essential for Notch pathway inhibition and muscle differentiation. Lastly, we report that, in vestigial mutants, fringe expression is lost, and when fringe is overexpressed, a significant rescue of indirect flight muscle degeneration is obtained. Altogether, our data show that a vestigial-differentiating function is achieved through the inhibition of the Notch pathway. [Copyright &y& Elsevier]

Abstract: Suppression of wing fate and specification of haltere fate in Drosophila by the homeotic gene Ultrabithorax is a classical example of Hox regulation of serial homology (Lewis, E.B. 1978. Nature 276, 565–570) and has served as a paradigm for understanding homeotic gene function. We have used DNA microarray analyses to identify potential targets of Ultrabithorax function during haltere specification. Expression patterns of 18 validated target genes and functional analyses of a subset of these genes suggest that down-regulation of both anterior–posterior and dorso-ventral signaling is critical for haltere fate specification. This is further confirmed by the observation that combined over-expression of Decapentaplegic and Vestigial is sufficient to override the effect of Ubx and cause dramatic haltere-to-wing transformations. Our results also demonstrate that analysis of the differential development of wing and haltere is a good assay system to identify novel regulators of key signaling pathways. [Copyright &y& Elsevier]

Abstract: The transcription factor Suppressor of Hairless (Su(H)) belongs to the CSL transcription factor family, which are the main transcriptional effectors of the Notch-signaling pathway. Su(H) is the only family member in the Drosophila genome and should therefore be the main transcriptional effector of the Notch pathway in this species. Despite this fact, in many developmental situations, the phenotype caused by loss of function of Su(H) is too weak for a factor that is supposed to mediate most or all aspects of Notch signaling. One example is the Su(H) mutant phenotype during the development of the wing, which is weaker in comparison to other genes required for Notch signaling. Another example is the complete absence of a phenotype upon loss of Su(H) function during the formation of the dorsoventral (D/V) compartment boundary, although the Notch pathway is required for this process. Recent work has shown that Su(H)/CBF1 has a second function as a transcriptional repressor, in the absence of the activity of the Notch pathway. As a repressor, Su(H) acts in a complex together with Hairless (H), which acts as a bridge to recruit the co-repressors Groucho and CtBP, and acts in a Notch-independent manner to prevent the transcription of target genes. This raises the possibility that a de-repression of target genes can occur in the case of loss if function of Su(H). Here, we show that the weak phenotype of Su(H) mutants during wing development and the absence of a phenotype during formation of the D/V compartment boundary are caused by the concomitant loss of the Notch-independent repressor function. This loss of the repressor function of Su(H) results in a de-repression of expression of target genes to a different degree in each process. Loss of Su(H) function during wing development results in a transient de-repression of expression of the selector gene vestigial (vg). We show that this residual expression of vg is responsible for the weaker mutant phenotype of Su(H) in the wing. During the formation of the D/V compartment boundary, de-repression of target genes seems to be sufficiently strong, to compensate the loss of Su(H) activity. Thus, de-repression of its target genes obscures the involvement of Su(H) in this process. Furthermore, we provide evidence that Dx does not signal in a Su(H)-independent manner as has been suggested previously. [Copyright &y& Elsevier]

Abstract: The conjugation of the ubiquitin-like protein SUMO to lysine side chains plays widespread roles in the regulation of nuclear protein function. Since little information is available about the roles of SUMO in development, we have screened a collection of chromosomal deficiencies to identify developmental processes regulated by SUMO. We found that flies heterozygous for a deficiency uncovering vestigial (vg) and mutations in any of several genes encoding components of the SUMO conjugation machinery exhibit severe wing notching. This phenotype is due to an interaction between sumo and vg since it is suppressed by expression of Vg from a transgene, and is also observed in flies doubly heterozygous for vg hypomorphic alleles and sumo. In addition, the ability of Vg to direct the formation of ectopic wings when misexpressed in the eye field is enhanced by simultaneous misexpression of SUMO. In S2 cell transient transfection assays, overexpression of SUMO and the SUMO conjugating enzyme Ubc9, but not a catalytically inactive form of Ubc9, results in sumoylation of Vg and augments the activation of a Vg-responsive reporter. These findings are consistent with the idea that sumoylation stimulates Vg function during wing morphogenesis. [Copyright &y& Elsevier]

Scalloped (SD) and Vestigial (VG) proteins physically interact to form a selector complex that activates genes involved in wing development in Drosophila melanogaster. SD belongs to a conserved family of transcription factors containing the TEA/ATTS DNA-binding motif. VG is also a nuclear protein providing the activator function for the SD VG complex. The TEA DNA-binding domain and the VG interacting domain (VID) of SD have been previously identified and described. However, they, and possibly other functional domains of SD, have not been thoroughly characterized in vivo. Herein, transgenic constructs encoding various truncations of SD were used to assess their respective ability to rescue the mutant wing phenotype of two viable sd recessive mutations (sdETX4 and sd58d). The transgenic strains produced were also tested for the ability to induce further sd expression, an ability possessed by full length SD. The functional dissection of SD confirms that specific regions are necessary for wing development and provides further information as to how the SD VG complex functions to promote wing fate. Previous experiments have shown that expression of full length SD can cause a dominant negative wing phenotype. We show that expression of constructs that delete the SD DNA-binding domain can also cause a dominant negative phenotype in a background with either of the two tester sd strains. In contrast, SD constructs that delete the VID have no effect on the wing phenotype in either tester background. Finally, a significant portion of SD at the N-terminal end appears to be dispensable with respect to normal wing development, as this construct behaves the same as full length SD in our assays. [ABSTRACT FROM AUTHOR]

The development of the Drosophila wing is governed by the action of two morphogens encoded by the genes decapentaplegic (dpp; a member of the BMP gene family) and wingless (wg; a member of the WNT gene family), which promote cell proliferation and pattern the wing. Along the anterior/posterior (A/P) axis, the precise expression of decapentaplegic and its receptors is required for the transcriptional regulation of specific target genes. In the present work, we analyze the function of the T-box gene optomotor-blind (omb), a decapentaplegic target gene. The wings of optomotor-blind mutants have two apparently opposite phenotypes: the central wing is severely reduced and shows massive cell death, mainly in the distal-most wing, and the lateral wing shows extra cell proliferation. Here, we present genetic evidence that optomotor-blind is required to establish the graded expression of the decapentaplegic type I receptor encoded by the gene thick veins (tkv) to repress the expression of the gene master of thickveins and also to activate the expression of spalt (sal) and vestigial (vg), two decapentaplegic target genes. optomotor-blind plays a role in wing development downstream of decapentaplegic by controlling the expression of its receptor thick veins and by mediating the activation of target genes required for the correct development of the wing. The lack of optomotor-blind produces massive cell death in its expression domain, which leads to the mis-activation of the Notch pathway and the overproliferation of lateral wing cells. [Copyright &y& Elsevier]

Drosophila thoracic muscles are comprised of both direct flight muscles (DFMs) and indirect flight muscles (IFMs). The IFMs can be further subdivided into dorsolongitudinal muscles (DLMs) and dorsoventral muscles (DVMs). The correct patterning of each category of muscles requires the coordination of specific executive regulatory programs. DFM development requires key regulatory genes such as cut (ct) and apterous (ap), whereas IFM development requires vestigial (vg). Using a new vgnull mutant, we report that a total absence of vg leads to DLM degeneration through an apoptotic process and to a total absence of DVMs in the adult. We show that vg and scalloped (sd), the only known VG transcriptional coactivator, are coexpressed during IFM development. Moreover, we observed an ectopic expression of ct and ap, two markers of DFM development, in developing IFMs of vgnull pupae. In addition, in vgnull adult flies, degenerating DLMs express twist (twi) ectopically. We provide evidence that ap ectopic expression can induce per se ectopic twi expression and muscle degeneration. All these data seem to indicate that, in the absence of vg, the IFM developmental program switches into the DFM developmental program. Moreover, we were able to rescue the muscle phenotype of vgnull flies by using the activity of ap promoter to drive VG expression. Thus, vg appears to be a key regulatory gene of IFM development. [Copyright &y& Elsevier]

The Drosophila homologue of the human TEF-1 gene, scalloped (sd), is required for wing development. The SD protein forms part of a transcriptional activation complex with the protein encoded by vestigial (vg) that, in turn, activates target genes important for wing formation. One sd function involves a regulatory feedback loop with vg and wingless (wg) that is essential in this process. The dorsal–ventral (D/V) margin-specific expression of wg is lost in sd mutant wing discs while the hinge-specific expression appears normal. In the context of wing development, a vg::sdTEA domain fusion produces a protein that mimics the wild-type SD/VG complex and restores the D/V boundary-specific expression of wg in a sd mutant background. Further, targeted expression of wg at the D/V boundary in the wing disc was able to partially rescue the sd mutant phenotype. This infers that sd could function in either the maintenance or induction of wg at the D/V border. Another functional role for sd is the establishment of sensory organ precursors (SOP) of the peripheral nervous system at the wing margin. Thus, the relationship between sd and senseless (sens) in the development of these cells is also examined, and it appears that sd must be functional for proper sens expression, and ultimately, for sensory organ precursor development. [Copyright &y& Elsevier]

Electron-pair density wave (PDW) states are now an intense focus of research in the field of cuprate correlated superconductivity. PDWs exhibit periodically modulating superconductive electron pairing that can be visualized directly using scanned Josephson tunneling microscopy (SJTM). Although from theory, intertwining the d -wave superconducting (DSC) and PDW order parameters allows a plethora of global electron-pair orders to appear, which one actually occurs in the various cuprates is unknown. Here, we use SJTM to visualize the interplay of PDW and DSC states in Bi 2 Sr 2 CaCu 2 O 8+x at a carrier density where the charge density wave modulations are virtually nonexistent. Simultaneous visualization of their amplitudes reveals that the intertwined PDW and DSC are mutually attractive states. Then, by separately imaging the electron-pair density modulations of the two orthogonal PDWs, we discover a robust nematic PDW state. Its spatial arrangement entails Ising domains of opposite nematicity, each consisting primarily of unidirectional and lattice commensurate electron-pair density modulations. Further, we demonstrate by direct imaging that the scattering resonances identifying Zn impurity atom sites occur predominantly within boundaries between these domains. This implies that the nematic PDW state is pinned by Zn atoms, as was recently proposed [Lozano et al. , Phys. Rev. B 103, L020502 (2021)]. Taken in combination, these data indicate that the PDW in Bi 2 Sr 2 CaCu 2 O 8+x is a vestigial nematic pair density wave state [Agterberg et al. Phys. Rev. B 91, 054502 (2015); Wardh and Granath arXiv:2203.08250].

The development of the Drosophila wing involves progressive patterning events. In the second larval instar, cells of the wing disc are allotted wing or notum fates by a wingless-mediated process and dorsal or ventral fates by the action of apterous and wingless. Notch-mediated signalling is required for the expression of the genes vestigial and scalloped in the presumptive wing blade. Later, wingless, Notch and cut are involved in cell fate specification along the wing margin. The function of scalloped in this process is not well understood and is the focus of this study. We show that patterning downstream of Notch and wingless pathways is altered in scalloped mutants. Reduction in scalloped expression results in a loss of expression of wing blade- and margin-specific markers. Misexpression of scalloped in the presumptive wing causes misexpression of scalloped, vestigial and wingless reporter genes. However, high levels of scalloped expression have a negative influence on wingless, vestigial and its own expression. Our results demonstrate that scalloped functions in a level-dependent manner in the presumptive wing blade in a loop that involves vestigial and itself. We suggest that wing development requires the regulated expression of scalloped together with vestigial–the ”wing formation” effects of Vestigial in other imaginal discs are probably due to its interaction with the scalloped gene product normally expressed in these discs. [ABSTRACT FROM AUTHOR]

The two genes vestigial ( vg) and scalloped ( sd) are required for wing development in Drosophila melanogaster. They present similar patterns of expression in second and third instar wing discs and similar wing mutant phenotypes . vg encodes a nuclear protein without any recognized nucleic acid-binding motif. Sd is a transcription factor homologous to the human TEF-1 factor whose promoter activity depends on cell-specific cofactors. We postulate that Vg could be a cofactor of Sd in the wing morphogenetic process and that, together, they could constitute a functional transcription complex. We investigated genetic interactions between the two genes. We show here that vg and sd co-operate in vivo in a manner dependent on the structure of the Vg protein. We ectopically expressed vg in the patch ( ptc) domains. We show evidence that wing-like outgrowths induced by ectopic expression of vg are severely reduced in vg or sd mutant backgrounds. Accordingly, we demonstrate that ptc-GAL4-driven expression of vg induces both expressions of the endogenous vg and sd genes and that the two Vg and Sd proteins have to be produced together to promote wing proliferation. Futhermore, we show an interaction between the two proteins by double hybrid experiments in yeast. Our results therefore support the hypothesis that Sd and Vg directly interact in vivo to form a complex regulating the proliferation of wing tissue. [ABSTRACT FROM AUTHOR]

During the evolutionary history of flowering plants, transitions between pollinator groups (pollinator shifts) have been frequent, 1 and contributed to the spectacular radiation of angiosperms. 2 Although the evolution of floral traits during pollinator shifts has been studied in real time under controlled laboratory conditions, 3 it is challenging to study in nature and therefore poorly understood. 4–7 Using a comparative, multidisciplinary approach, we dissect the evolution of floral traits during a pollinator shift in the long-spurred African orchid Satyrium longicauda. Phylogenetic analysis and ecological experiments revealed a shift from moth- to oil-collecting bee pollination. Remarkably, flowers of the bee-pollinated form are similar in morphology, color, and overall volatile chemistry to those of moth-pollinated forms, but differ in having spurs that are mostly devoid of nectar, and have an elevated presence of the oil-derived compound diacetin, which oil-collecting bees use as a cue for oil presence. 8 Experiments demonstrated that long spurs are critical for pollination of a moth-pollinated form, but are not needed for pollination of the bee-pollinated form. We conclude that the pollinator shift in Satyrium was mediated by a switch in chemistry of the pollinator reward. The ancestral presence of diacetin might have served as a pre-adaptation for bee pollination, whereas the current mismatch between flower morphology and bees is due to the retention of vestigial floral spurs. These results elucidate the sequence of floral evolution in the early stages of pollinator shifts and help to explain the assembly of suites of co-varying traits through pre-adaptation and vestigialization. 9–12 • Satyrium longicauda is characterized by two pollination ecotypes • Pollination by oil-collecting bees is derived from moth pollination • The pollinator shift process is associated with pre-adaptation and vestigialization • Minor modifications in floral chemistry can initiate major pollinator shifts Pollinator shifts were frequent in angiosperms, but how do they happen? Castañeda-Zárate et al. study "evolution-in-action" in an African orchid. They reconstruct a novel shift from moth- to oil-collecting bee pollination. The bee-pollinated form resembles moth-pollinated forms, but produces oil instead of nectar, driving the pollinator shift. [ABSTRACT FROM AUTHOR]