13 results on '"Yamamoto, Shinya"'
Search Results
2. Functional Studies of Genetic Variants Associated with Human Diseases in Notch Signaling-Related Genes Using Drosophila.
- Author
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Yang SA, Salazar JL, Li-Kroeger D, and Yamamoto S
- Subjects
- Animals, Exome, Genetic Predisposition to Disease, Genomics methods, Humans, Phenotype, Drosophila genetics, Drosophila melanogaster genetics
- Abstract
Rare variants in the many genes related to Notch signaling cause diverse Mendelian diseases that affect myriad organ systems. In addition, genome- and exome-wide association studies have linked common and rare variants in Notch-related genes to common diseases and phenotypic traits. Moreover, somatic mutations in these genes have been observed in many types of cancer, some of which are classified as oncogenic and others as tumor suppressive. While functional characterization of some of these variants has been performed through experimental studies, the number of "variants of unknown significance" identified in patients with diverse conditions keeps increasing as high-throughput sequencing technologies become more commonly used in the clinic. Furthermore, as disease gene discovery efforts identify rare variants in human genes that have yet to be linked to a disease, the demand for functional characterization of variants in these "genes of unknown significance" continues to increase. In this chapter, we describe a workflow to functionally characterize a rare variant in a Notch signaling related gene that was found to be associated with late-onset Alzheimer's disease. This pipeline involves informatic analysis of the variant of interest using diverse human and model organism databases, followed by in vivo experiments in the fruit fly Drosophila melanogaster. The protocol described here can be used to study variants that affect amino acids that are not conserved between human and fly. By "humanizing" the almondex gene in Drosophila with mutant alleles and heterologous genomic rescue constructs, a missense variant in TM2D3 (TM2 Domain Containing 3) was shown to be functionally damaging. This, and similar approaches, greatly facilitate functional interpretations of genetic variants in the human genome and propel personalized medicine., (© 2022. The Author(s), under exclusive license to Springer Science+Business Media, LLC, part of Springer Nature.)
- Published
- 2022
- Full Text
- View/download PDF
3. De Novo Variants in WDR37 Are Associated with Epilepsy, Colobomas, Dysmorphism, Developmental Delay, Intellectual Disability, and Cerebellar Hypoplasia.
- Author
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Kanca, Oguz, Andrews, Jonathan C, Lee, Pei-Tseng, Patel, Chirag, Braddock, Stephen R, Slavotinek, Anne M, Cohen, Julie S, Gubbels, Cynthia S, Aldinger, Kimberly A, Williams, Judy, Indaram, Maanasa, Fatemi, Ali, Yu, Timothy W, Agrawal, Pankaj B, Vezina, Gilbert, Simons, Cas, Crawford, Joanna, Lau, C Christopher, Undiagnosed Diseases Network, Chung, Wendy K, Markello, Thomas C, Dobyns, William B, Adams, David R, Gahl, William A, Wangler, Michael F, Yamamoto, Shinya, Bellen, Hugo J, and Malicdan, May Christine V
- Subjects
Undiagnosed Diseases Network ,Cerebellum ,Animals ,Humans ,Drosophila melanogaster ,Epilepsy ,Nervous System Malformations ,Coloboma ,Microfilament Proteins ,Developmental Disabilities ,Amino Acid Sequence ,Sequence Homology ,Phenotype ,Mutation ,Adult ,Child ,Infant ,Infant ,Newborn ,Female ,Male ,Young Adult ,Body Dysmorphic Disorders ,Intellectual Disability ,WD40 Repeats ,CG12333 ,Drosophila ,WD40 repeats ,WDR37 domains ,bang sensitivity ,wdr37 ,Genetics ,Pediatric ,Rare Diseases ,Congenital Structural Anomalies ,Neurodegenerative ,Neurosciences ,Brain Disorders ,Intellectual and Developmental Disabilities (IDD) ,Aetiology ,2.1 Biological and endogenous factors ,Neurological ,Biological Sciences ,Medical and Health Sciences ,Genetics & Heredity - Abstract
WD40 repeat-containing proteins form a large family of proteins present in all eukaryotes. Here, we identified five pediatric probands with de novo variants in WDR37, which encodes a member of the WD40 repeat protein family. Two probands shared one variant and the others have variants in nearby amino acids outside the WD40 repeats. The probands exhibited shared phenotypes of epilepsy, colobomas, facial dysmorphology reminiscent of CHARGE syndrome, developmental delay and intellectual disability, and cerebellar hypoplasia. The WDR37 protein is highly conserved in vertebrate and invertebrate model organisms and is currently not associated with a human disease. We generated a null allele of the single Drosophila ortholog to gain functional insights and replaced the coding region of the fly gene CG12333/wdr37 with GAL4. These flies are homozygous viable but display severe bang sensitivity, a phenotype associated with seizures in flies. Additionally, the mutant flies fall when climbing the walls of the vials, suggesting a defect in grip strength, and repeat the cycle of climbing and falling. Similar to wall clinging defect, mutant males often lose grip of the female abdomen during copulation. These phenotypes are rescued by using the GAL4 in the CG12333/wdr37 locus to drive the UAS-human reference WDR37 cDNA. The two variants found in three human subjects failed to rescue these phenotypes, suggesting that these alleles severely affect the function of this protein. Taken together, our data suggest that variants in WDR37 underlie a novel syndromic neurological disorder.
- Published
- 2019
4. Loss of Nardilysin, a Mitochondrial Co-chaperone for α-Ketoglutarate Dehydrogenase, Promotes mTORC1 Activation and Neurodegeneration
- Author
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Yoon, Wan Hee, Sandoval, Hector, Nagarkar-Jaiswal, Sonal, Jaiswal, Manish, Yamamoto, Shinya, Haelterman, Nele A, Putluri, Nagireddy, Putluri, Vasanta, Sreekumar, Arun, Tos, Tulay, Aksoy, Ayse, Donti, Taraka, Graham, Brett H, Ohno, Mikiko, Nishi, Eiichiro, Hunter, Jill, Muzny, Donna M, Carmichael, Jason, Shen, Joseph, Arboleda, Valerie A, Nelson, Stanley F, Wangler, Michael F, Karaca, Ender, Lupski, James R, and Bellen, Hugo J
- Subjects
Biological Psychology ,Biomedical and Clinical Sciences ,Neurosciences ,Psychology ,Neurodegenerative ,Genetics ,Animals ,Autophagy ,Drosophila ,Drosophila Proteins ,Drosophila melanogaster ,Ketoglutarate Dehydrogenase Complex ,Ketoglutaric Acids ,Lysine ,Mechanistic Target of Rapamycin Complex 1 ,Metalloendopeptidases ,Mitochondria ,Molecular Chaperones ,Multiprotein Complexes ,Neurodegenerative Diseases ,TOR Serine-Threonine Kinases ,DNAJA3 ,NRD1 ,OGDHL ,TCA cycle ,alpha-ketoglutarate ,autophagy ,metabolism ,mitochondrial chaperones ,rapamycin ,Cognitive Sciences ,Neurology & Neurosurgery ,Biological psychology - Abstract
We previously identified mutations in Nardilysin (dNrd1) in a forward genetic screen designed to isolate genes whose loss causes neurodegeneration in Drosophila photoreceptor neurons. Here we show that NRD1 is localized to mitochondria, where it recruits mitochondrial chaperones and assists in the folding of α-ketoglutarate dehydrogenase (OGDH), a rate-limiting enzyme in the Krebs cycle. Loss of Nrd1 or Ogdh leads to an increase in α-ketoglutarate, a substrate for OGDH, which in turn leads to mTORC1 activation and a subsequent reduction in autophagy. Inhibition of mTOR activity by rapamycin or partially restoring autophagy delays neurodegeneration in dNrd1 mutant flies. In summary, this study reveals a novel role for NRD1 as a mitochondrial co-chaperone for OGDH and provides a mechanistic link between mitochondrial metabolic dysfunction, mTORC1 signaling, and impaired autophagy in neurodegeneration.
- Published
- 2017
5. Comparative exploration of mammalian deafness gene homologues in the Drosophila auditory organ shows genetic correlation between insect and vertebrate hearing.
- Author
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Sutton, Daniel C., Andrews, Jonathan C., Dolezal, Dylan M., Park, Ye Jin, Li, Hongjie, Eberl, Daniel F., Yamamoto, Shinya, and Groves, Andrew K.
- Subjects
GENETIC correlations ,DEAFNESS ,CORTI'S organ ,DROSOPHILA melanogaster ,FRUIT flies ,DROSOPHILA ,DROSOPHILIDAE - Abstract
Johnston's organ, the Drosophila auditory organ, is anatomically very different from the mammalian organ of Corti. However, recent evidence indicates significant cellular and molecular similarities exist between vertebrate and invertebrate hearing, suggesting that Drosophila may be a useful platform to determine the function of the many mammalian deafness genes whose underlying biological mechanisms are poorly characterized. Our goal was a comprehensive screen of all known orthologues of mammalian deafness genes in the fruit fly to better understand conservation of hearing mechanisms between the insect and the fly and ultimately gain insight into human hereditary deafness. We used bioinformatic comparisons to screen previously reported human and mouse deafness genes and found that 156 of them have orthologues in Drosophila melanogaster. We used fluorescent imaging of T2A-GAL4 gene trap and GFP or YFP fluorescent protein trap lines for 54 of the Drosophila genes and found 38 to be expressed in different cell types in Johnston's organ. We phenotypically characterized the function of strong loss-of-function mutants in three genes expressed in Johnston's organ (Cad99C, Msp-300, and Koi) using a courtship assay and electrophysiological recordings of sound-evoked potentials. Cad99C and Koi were found to have significant courtship defects. However, when we tested these genes for electrophysiological defects in hearing response, we did not see a significant difference suggesting the courtship defects were not caused by hearing deficiencies. Furthermore, we used a UAS/RNAi approach to test the function of seven genes and found two additional genes, CG5921 and Myo10a, that gave a statistically significant delay in courtship but not in sound-evoked potentials. Our results suggest that many mammalian deafness genes have Drosophila homologues expressed in the Johnston's organ, but that their requirement for hearing may not necessarily be the same as in mammals. [ABSTRACT FROM AUTHOR]
- Published
- 2024
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- View/download PDF
6. TM2D genes regulate Notch signaling and neuronal function in Drosophila.
- Author
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Salazar, Jose L., Yang, Sheng-An, Lin, Yong Qi, Li-Kroeger, David, Marcogliese, Paul C., Deal, Samantha L., Neely, G. Gregory, and Yamamoto, Shinya
- Subjects
NOTCH genes ,HUMAN genetics ,DROSOPHILA ,GENE families ,DROSOPHILA melanogaster ,APOLIPOPROTEIN E4 - Abstract
TM2 domain containing (TM2D) proteins are conserved in metazoans and encoded by three separate genes in each model organism species that has been sequenced. Rare variants in TM2D3 are associated with Alzheimer's disease (AD) and its fly ortholog almondex is required for embryonic Notch signaling. However, the functions of this gene family remain elusive. We knocked-out all three TM2D genes (almondex, CG11103/amaretto, CG10795/biscotti) in Drosophila and found that they share the same maternal-effect neurogenic defect. Triple null animals are not phenotypically worse than single nulls, suggesting these genes function together. Overexpression of the most conserved region of the TM2D proteins acts as a potent inhibitor of Notch signaling at the γ-secretase cleavage step. Lastly, Almondex is detected in the brain and its loss causes shortened lifespan accompanied by progressive motor and electrophysiological defects. The functional links between all three TM2D genes are likely to be evolutionarily conserved, suggesting that this entire gene family may be involved in AD. Author summary: Alzheimer's disease (AD) is the most common neurodegenerative disease affecting the aging population. Although many genetic factors have been implicated in its pathogenesis, in vivo functions of many of these genes have not been well defined. In this study, we investigated the function of TM2D3, a conserved gene that has been implicated in late-onset AD through an exome-wide association study, and two closely related genes, TM2D1 and TM2D2, using the fruit fly Drosophila melanogaster. In addition to exhibiting a previously reported maternal-effect neuurodevelopmental phenotype caused by Notch signaling defects during embryogenesis, fly TM2D3 mutants are short lived and display age-dependent motor and electrophysiological defects, providing the first link between this gene and age-dependent neurological phenotypes. Furthermore, TM2D1 and TM2D2 knockout flies phenotypically mimic the loss of TM2D3. Triple knockout of all three TM2D genes resemble the single knockouts, suggesting that these genes likely function together. Together with functional data that implicates TM2D3 in a biological process that is liked to the γ-secretase, a protease that is involved in AD in addition to being required for proper Notch signaling, we propose that all three TM2D family genes may be involved in AD pathogenesis, which warrants further investigation through human genetics studies. [ABSTRACT FROM AUTHOR]
- Published
- 2021
- Full Text
- View/download PDF
7. Dopamine Dynamics and Signaling in Drosophila: An Overview of Genes, Drugs and Behavioral Paradigms
- Author
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Yamamoto, Shinya and Seto, Elaine S.
- Subjects
Neurotransmitter Agents ,Behavior, Animal ,Models, Genetic ,behavior ,Pigmentation ,Dopamine ,fungi ,Genes, Insect ,Review ,Pigments, Biological ,Motor Activity ,Circadian Rhythm ,Rats ,Mice ,Cognition ,Drosophila melanogaster ,Memory ,cuticle pigmentation ,Animals ,Humans ,Insect Proteins ,Learning ,Drosophila ,genetics ,Signal Transduction - Abstract
Changes in dopamine (DA) signaling have been implicated in a number of human neurologic and psychiatric disorders. Similarly, defects in DA signaling in the fruit fly, Drosophila melanogaster, have also been associated with several behavioral defects. As most genes involved in DA synthesis, transport, secretion, and signaling are conserved between species, Drosophila is a powerful genetic model organism to study the regulation of DA signaling in vivo. In this review, we will provide an overview of the genes and drugs that regulate DA biology in Drosophila. Furthermore, we will discuss the behavioral paradigms that are regulated by DA signaling in flies. By analyzing the genes and neuronal circuits that govern such behaviors using sophisticated genetic, pharmacologic, electrophysiologic, and imaging approaches in Drosophila, we will likely gain a better understanding about how this neuromodulator regulates motor tasks and cognition in humans.
- Published
- 2014
8. Making sense out of missense mutations: Mechanistic dissection of Notch receptors through structure‐function studies in Drosophila.
- Author
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Yamamoto, Shinya
- Subjects
- *
NOTCH genes , *NOTCH signaling pathway , *MISSENSE mutation , *SOMATIC mutation , *GENETIC testing , *DROSOPHILA , *ALLELES - Abstract
Notch signaling is involved in the development of almost all organ systems and is required post‐developmentally to modulate tissue homeostasis. Rare variants in Notch signaling pathway genes are found in patients with rare Mendelian disorders, while unique or recurrent somatic mutations in a similar set of genes are identified in cancer. The human genome contains four genes that encode Notch receptors, NOTCH1‐4, all of which are linked to genetic diseases and cancer. Although some mutations have been classified as clear loss‐ or gain‐of‐function alleles based on cellular or rodent based assay systems, the functional consequence of many variants/mutations in human Notch receptors remain unknown. In this review, I will first provide an overview of the domain structure of Notch receptors and discuss how each module is known to regulate Notch signaling activity in vivo using the Drosophila Notch receptor as an example. Next, I will introduce some interesting mutant alleles that have been isolated in the fly Notch gene over the past > 100 years of research and discuss how studies of these mutations have facilitated the understanding of Notch biology. By identifying unique alleles of the fly Notch gene through forward genetic screens, mapping their molecular lesions and characterizing their phenotypes in depth, one can begin to unravel new mechanistic insights into how different domains of Notch fine‐tune signaling output. Such information can be useful in deciphering the functional consequences of rare variants/mutations in human Notch receptors, which in turn can influence disease management and therapy. [ABSTRACT FROM AUTHOR]
- Published
- 2020
- Full Text
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9. Unraveling Novel Mechanisms of Neurodegeneration Through a Large-Scale Forward Genetic Screen in Drosophila.
- Author
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Deal, Samantha L. and Yamamoto, Shinya
- Subjects
NEURODEGENERATION ,DROSOPHILA ,NEURONS ,ALZHEIMER'S disease ,X chromosome - Abstract
Neurodegeneration is characterized by progressive loss of neurons. Genetic and environmental factors both contribute to demise of neurons, leading to diverse devastating cognitive and motor disorders, including Alzheimer's and Parkinson's diseases in humans. Over the past few decades, the fruit fly, Drosophila melanogaster , has become an integral tool to understand the molecular, cellular and genetic mechanisms underlying neurodegeneration. Extensive tools and sophisticated technologies allow Drosophila geneticists to identify and study evolutionarily conserved genes that are essential for neural maintenance. In this review, we will focus on a large-scale mosaic forward genetic screen on the fly X-chromosome that led to the identification of a number of essential genes that exhibit neurodegenerative phenotypes when mutated. Most genes identified from this screen are evolutionarily conserved and many have been linked to human diseases with neurological presentations. Systematic electrophysiological and ultrastructural characterization of mutant tissue in the context of the Drosophila visual system, followed by a series of experiments to understand the mechanism of neurodegeneration in each mutant led to the discovery of novel molecular pathways that are required for neuronal integrity. Defects in mitochondrial function, lipid and iron metabolism, protein trafficking and autophagy are recurrent themes, suggesting that insults that eventually lead to neurodegeneration may converge on a set of evolutionarily conserved cellular processes. Insights from these studies have contributed to our understanding of known neurodegenerative diseases such as Leigh syndrome and Friedreich's ataxia and have also led to the identification of new human diseases. By discovering new genes required for neural maintenance in flies and working with clinicians to identify patients with deleterious variants in the orthologous human genes, Drosophila biologists can play an active role in personalized medicine. [ABSTRACT FROM AUTHOR]
- Published
- 2019
- Full Text
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10. Clinically severe CACNA1A alleles affect synaptic function and neurodegeneration differentially.
- Author
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Luo, Xi, Rosenfeld, Jill A., Yamamoto, Shinya, Harel, Tamar, Zuo, Zhongyuan, Hall, Melissa, Wierenga, Klaas, Pastore, Matthew T., Bartholomew, Dennis, Delgado, Mauricio R., Rotenberg, Joshua, Lewis, Richard Alan, Emrick, Lisa, Bacino, Carlos A., Eldomery, Mohammad K., Coban Akdemir, Zeynep, Xia, Fan, Yang, Yaping, Lalani, Seema R., and Lotze, Timothy
- Subjects
DEVELOPMENTAL delay ,ATAXIA ,DROSOPHILA genetics ,ALLELES ,NEURODEGENERATION ,DEGENERATION (Pathology) ,GENETICS ,INSECTS - Abstract
Dominant mutations in CACNA1A, encoding the α-1A subunit of the neuronal P/Q type voltage-dependent Ca
2+ channel, can cause diverse neurological phenotypes. Rare cases of markedly severe early onset developmental delay and congenital ataxia can be due to de novo CACNA1A missense alleles, with variants affecting the S4 transmembrane segments of the channel, some of which are reported to be loss-of-function. Exome sequencing in five individuals with severe early onset ataxia identified one novel variant (p.R1673P), in a girl with global developmental delay and progressive cerebellar atrophy, and a recurrent, de novo p.R1664Q variant, in four individuals with global developmental delay, hypotonia, and ophthalmologic abnormalities. Given the severity of these phenotypes we explored their functional impact in Drosophila. We previously generated null and partial loss-of-function alleles of cac, the homolog of CACNA1A in Drosophila. Here, we created transgenic wild type and mutant genomic rescue constructs with the two noted conserved point mutations. The p.R1673P mutant failed to rescue cac lethality, displayed a gain-of-function phenotype in electroretinograms (ERG) recorded from mutant clones, and evolved a neurodegenerative phenotype in aging flies, based on ERGs and transmission electron microscopy. In contrast, the p.R1664Q variant exhibited loss of function and failed to develop a neurodegenerative phenotype. Hence, the novel R1673P allele produces neurodegenerative phenotypes in flies and human, likely due to a toxic gain of function. [ABSTRACT FROM AUTHOR]- Published
- 2017
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11. Rare Functional Variant in TM2D3 is Associated with Late-Onset Alzheimer's Disease.
- Author
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Jakobsdottir, Johanna, van der Lee, Sven J., Bis, Joshua C., Chouraki, Vincent, Li-Kroeger, David, Yamamoto, Shinya, Grove, Megan L., Naj, Adam, Vronskaya, Maria, Salazar, Jose L., DeStefano, Anita L., Brody, Jennifer A., Smith, Albert V., Amin, Najaf, Sims, Rebecca, Ibrahim-Verbaas, Carla A., Choi, Seung-Hoan, Satizabal, Claudia L., Lopez, Oscar L., and Beiser, Alexa
- Subjects
GENETICS of Alzheimer's disease ,ALZHEIMER'S disease treatment ,DISEASE susceptibility ,CELLULAR signal transduction ,NOTCH signaling pathway - Abstract
We performed an exome-wide association analysis in 1393 late-onset Alzheimer’s disease (LOAD) cases and 8141 controls from the CHARGE consortium. We found that a rare variant (P155L) in TM2D3 was enriched in Icelanders (~0.5% versus <0.05% in other European populations). In 433 LOAD cases and 3903 controls from the Icelandic AGES sub-study, P155L was associated with increased risk and earlier onset of LOAD [odds ratio (95% CI) = 7.5 (3.5–15.9), p = 6.6x10
-9 ]. Mutation in the Drosophila TM2D3 homolog, almondex, causes a phenotype similar to loss of Notch/Presenilin signaling. Human TM2D3 is capable of rescuing these phenotypes, but this activity is abolished by P155L, establishing it as a functionally damaging allele. Our results establish a rare TM2D3 variant in association with LOAD susceptibility, and together with prior work suggests possible links to the β-amyloid cascade. [ABSTRACT FROM AUTHOR]- Published
- 2016
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12. Ubr3, a Novel Modulator of Hh Signaling Affects the Degradation of Costal-2 and Kif7 through Poly-ubiquitination.
- Author
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Li, Tongchao, Fan, Junkai, Blanco-Sánchez, Bernardo, Giagtzoglou, Nikolaos, Lin, Guang, Yamamoto, Shinya, Jaiswal, Manish, Chen, Kuchuan, Zhang, Jie, Wei, Wei, Lewis, Michael T., Groves, Andrew K., Westerfield, Monte, Jia, Jianhang, and Bellen, Hugo J.
- Subjects
HEDGEHOG signaling proteins ,HOMEOSTASIS ,UBIQUITINATION ,DROSOPHILA ,SENSORY neurons - Abstract
Hedgehog (Hh) signaling regulates multiple aspects of metazoan development and tissue homeostasis, and is constitutively active in numerous cancers. We identified Ubr3, an E3 ubiquitin ligase, as a novel, positive regulator of Hh signaling in Drosophila and vertebrates. Hh signaling regulates the Ubr3-mediated poly-ubiquitination and degradation of Cos2, a central component of Hh signaling. In developing Drosophila eye discs, loss of ubr3 leads to a delayed differentiation of photoreceptors and a reduction in Hh signaling. In zebrafish, loss of Ubr3 causes a decrease in Shh signaling in the developing eyes, somites, and sensory neurons. However, not all tissues that require Hh signaling are affected in zebrafish. Mouse UBR3 poly-ubiquitinates Kif7, the mammalian homologue of Cos2. Finally, loss of UBR3 up-regulates Kif7 protein levels and decreases Hh signaling in cultured cells. In summary, our work identifies Ubr3 as a novel, evolutionarily conserved modulator of Hh signaling that boosts Hh in some tissues. [ABSTRACT FROM AUTHOR]
- Published
- 2016
- Full Text
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13. Drosophila as a Model for Infectious Diseases.
- Author
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Harnish, J. Michael, Link, Nichole, Yamamoto, Shinya, and Gupta, Bhagwati
- Subjects
COMMUNICABLE diseases ,DROSOPHILA ,DROSOPHILA melanogaster ,FRUIT flies ,MULTICELLULAR organisms - Abstract
The fruit fly, Drosophila melanogaster, has been used to understand fundamental principles of genetics and biology for over a century. Drosophila is now also considered an essential tool to study mechanisms underlying numerous human genetic diseases. In this review, we will discuss how flies can be used to deepen our knowledge of infectious disease mechanisms in vivo. Flies make effective and applicable models for studying host-pathogen interactions thanks to their highly conserved innate immune systems and cellular processes commonly hijacked by pathogens. Drosophila researchers also possess the most powerful, rapid, and versatile tools for genetic manipulation in multicellular organisms. This allows for robust experiments in which specific pathogenic proteins can be expressed either one at a time or in conjunction with each other to dissect the molecular functions of each virulent factor in a cell-type-specific manner. Well documented phenotypes allow large genetic and pharmacological screens to be performed with relative ease using huge collections of mutant and transgenic strains that are publicly available. These factors combine to make Drosophila a powerful tool for dissecting out host-pathogen interactions as well as a tool to better understand how we can treat infectious diseases that pose risks to public health, including COVID-19, caused by SARS-CoV-2. [ABSTRACT FROM AUTHOR]
- Published
- 2021
- Full Text
- View/download PDF
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