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Darwin's finches are the most classic case of evolution. Early studies on the evolution of this species were mainly based on morphology. Until now, the mitochondrial genome of Geospiza magnirostris has been sequenced and the study explored the characteristics of the complete genome of G. magnirostris and verified the evolutionary position of it. The 13 PCGs initiated by ATN codons. The stop codons of three PCGs (ND2, COX3 and ND4) were incomplete, with only T- or TA- replacing complete form TAA or TAG. All the tRNA genes expressed a typical cloverleaf secondary structure, except for tRNASer1(AGY), whose dihydrouridine (DHU) arm was lack and instead with a simple loop. In the sequence of the control region of G. magnirostris, we found six simple repeat tandem sequences with a total length of 42 bp. Two characteristic conserved overlapping junction (ATGCTAA) and (CAAGAAAG) were observed as reported for eight selected Passeriformes birds. A special conserved overlapping junction (ATCTTACC) involved in mitochondrial transcription termination was found between tRNATyr and COX1 in G. magnirostris's control region. Four most frequently used amino acids in G. magnirostris's PCGs were Leu1 (CUN), Ile, Thr, Ala. The codon usage of G. magnirostris was relatively average, and there was no particular bias. The ratio Ka/Ks results showed that G. magnirostris receives less natural selection pressure. The phylogenetic relationships and cluster analysis of relative codon usage showed that G. magnirostris and Thraupis episcopus clustered in one branch. The phylogenetic position of G. magnirostris was consistent with the traditional taxonomic of Thraupis. The results supported the conclusion that G. magnirostris belongs to the morphological classification of the family Thraupidae. [ABSTRACT FROM AUTHOR]

Background: Although transfer RNA (tRNA) has been found to be the main source of a rich class of noncoding RNA, the tRNA‐derived small RNA (tsRNA) has been proved to play an irreplaceable role in the human body, and its dynamic imbalance could affect the progress of the disease. However, the research on tsRNA in oral submucous fibrosis (OSF) is still scarce. Methods: We sequenced the OSF and validated it by PCR. We found that there were significant differences in their expression levels in OSF. Furthermore, bioinformatic analysis was performed to explore the roles of these fragments in oral submucous fibrosis. Results: Of 126 tsRNAs in OSF were dysregulated, including 73 upregulated tsRNAs and 53 downregulated tsRNAs. The downregulated tiRNA‐Val‐CAC‐002, tRF‐Asn‐GTT‐005, tRF‐Trp‐CCA‐007 and upregulated tRF‐Gly‐TCC‐016, tRF‐Pro‐TGG‐009 showed significant differences by qRT‐PCR validation, which were consistent with the results of RNA sequencing. Gene ontology and pathway analysis revealed that tRF‐Gly‐TCC‐016 would possibly promote the formation and progress of OSF through cytokine‐cytokine receptor interaction and cAMP signal pathway, while tiRNA‐Val‐CAC‐002 could be primarily concerned with the transition from OSF to oral squamous cell carcinoma (OSCC). Conclusion: tRNA‐derived fragments are dysregulated and could be involved in the pathogenesis of oral submucous fibrosis. tRF‐Gly‐TCC‐016 and tiRNA‐Val‐CAC‐002 may be new regulatory molecules that could affect the process of OSF by regulating signal pathways through interacting with multiple genes. [ABSTRACT FROM AUTHOR]

This present research work reports the comparative analysis of the entire nucleotide sequence of mitochondrial genomes of Serranochromis robustus and Buccochromis nototaenia and phylogenetic analyses of their protein-coding genes in order to establish their phylogenetic relationship within Cichlids. The mitochondrial genomes of S. robustus and B. nototaenia are 16,583 and 16,580 base pairs long, respectively, including 13 protein-coding genes (PCGs), 2 ribosomal RNA genes, 22 transfer RNA genes, and one control region (D-loop) which is 888 and 887 base pairs long, respectively, showing the same gene order and identical number of gene or regions with other well-elucidated mitogenomes of Cichlids. However, with exception of cytochrome-c oxidase subunit-1 (COX-1) gene, all the identified PCGs were initiated by ATG-codons. Structurally, 11 tRNA genes in B. nototaenia species and 9 tRNA genes in S. robustus species, folded into typical clover-leaf secondary structure created by the regions of self-complementarity within tRNA. All the 22 tRNA genes in both species lack variable loop. Moreover, 28 genes which include 12-protein-coding genes are encoded on the H-strand and the remaining 9 genes including one protein-coding gene are encoded on the L-strand. Thirteen sequences of concatenated mitochondrial protein-coding genes were aligned using MUSCLE, and the phylogenetic analyses performed using maximum likelihood and Bayesian inference showed that S. robustus and B. nototaenia had a broad phylogenetic relationship. These results may be a useful tool in resolving higher-level relationships in organisms and a useful dataset for studying the evolution of the Cichlidae mitochondrial genome, since Cichlids are well-known model species in the study of evolutionary biology, because of their extreme morphological, biogeographical, parental care behavior for eggs and larvae and phylogenetic diversities. [ABSTRACT FROM AUTHOR]

Highlights • Synanthropic rodents and shrews shed atypical EPEC (aEPEC), but not EHEC strains. • aEPEC strains of diverse origin can be lysogenized with a stx -depleted bacteriophage yielding stable, yet prophage-inducible lysogens. • Sequence comparison of two highly related murine and human aEPEC strains and their respective lysogens showed sequence identities of >90%. • Whole genome analysis revealed prophage integration into the highly variable tRNA integration site argW in all three lysogens. • aEPEC are progenitors of typical EHEC. Abstract Bacteriophages play an important role in the evolution of bacterial pathogens. A phage-mediated transfer of stx -genes to atypical enteropathogenic E. coli (aEPEC) which are prevalent in different hosts, would convert them to enterohemorrhagic E. coli (EHEC). We decided to confirm this hypothesis experimentally to provide conclusive evidence that aEPEC isolated from different mammalian hosts are indeed progenitors of typical EHEC which gain the ability to produce Shiga-Toxin by lysogeny with stx -converting bacteriophages, utilizing the model phage Φ3538 Δ stx 2 ::cat. We applied a modified in vitro plaque-assay, using a high titer of a bacteriophage carrying a deletion in the stx 2 gene (Φ3538 Δ stx 2 ::cat) to increase the detection of lysogenic conversion events. Three wild-type aEPEC strains were chosen as acceptor strains: the murine aEPEC-strain IMT14505 (sequence type (ST)28, serotype Ont:H6), isolated from a striped field mouse (Apodemus agrarius) in the surrounding of a cattle shed, and the human aEPEC-strain 910#00 (ST28, Ont:H6). The close genomic relationship of both strains implies a high zoonotic potential. A third strain, the bovine aEPEC IMT19981, was of serotype O26:H11 and ST21 (STC29). All three aEPEC were successfully lysogenized with phage Φ3538 Δ stx 2 ::cat. Integration of the bacteriophage DNA into the aEPEC host genomes was confirmed by amplification of chloramphenicol transferase (cat) marker gene and by Southern-Blot hybridization. Analysis of the whole genome sequence of each of the three lysogens showed that the bacteriophage was integrated into the known tRNA integration site argW , which is highly variable among E. coli. In conclusion, the successful lysogenic conversion of aEPEC with a stx -phage in vitro underlines the important role of aEPEC as progenitors of EHEC. Given the high prevalence and the wide host range of aEPEC acceptors, their high risk of zoonotic transmission should be recognized in infection control measures. [ABSTRACT FROM AUTHOR]

In this study, we isolated and characterized a lytic phage, named vB_SmaM_PS2 (abbreviated as PS2), which can infect Serratia marcescens clinical isolates. Morphologically, phage PS2 can be classified within the Myoviridae family. The 167,276 bp double-stranded DNA genome of PS2 possesses 41.7% GC content. A total of 276 protein-coding genes and 4 tRNA genes were predicted in the PS2 genome. Of the 276 genes, 131 (47%) encoded T4-like genes, most of which are DNA replication and virion structural genes. Therefore, phage PS2 should be a new member of the T4-like Serratia phage. [ABSTRACT FROM AUTHOR]

We isolated a Pseudomonas phage infecting Pseudomonas fluorescens SA1 separated from a soil sample collected in Sichuan Province, China. This phage, which we named PPSC2, has a genome that is composed of a 97,330-bp-long linear double-stranded DNA with 47.51% G+C content and 168 putative protein-coding genes. We identified 20 tRNA genes in the genome of PPSC2, and the tRNA GC content ranged from 44.2% to 58.4%. Phylogenetic and BLASTn analysis revealed that the Pseudomonas phage PPSC2 should be considered a new member of the family Myoviridae. [ABSTRACT FROM AUTHOR]

The succession of molecular events leading to eukaryotic translation reinitiation—whereby ribosomes terminate translation of a short open reading frame (ORF), resume scanning, and then translate a second ORF on the same mRNA—is not well understood. Density-regulated reinitiation and release factor (DENR) and multiple copies in T-cell lymphoma-1 (MCTS1) are implicated in promoting translation reinitiation both in vitro in translation extracts and in vivo. We present here the crystal structure of MCTS1 bound to a fragment of DENR. Based on this structure, we identify and experimentally validate that DENR residues Glu42, Tyr43, and Tyr46 are important for MCTS1 binding and that MCTS1 residue Phe104 is important for tRNA binding. Mutation of these residues reveals that DENR-MCTS1 dimerization and tRNA binding are both necessary for DENR and MCTS1 to promote translation reinitiation in human cells. These findings thereby link individual residues of DENR and MCTS1 to specific molecular functions of the complex. Since DENR–MCTS1 can bind tRNA in the absence of the ribosome, this suggests the DENR–MCTS1 complex could recruit tRNA to the ribosome during reinitiation analogously to the eukaryotic initiation factor 2 (eIF2) complex in cap-dependent translation. [ABSTRACT FROM AUTHOR]

Coccidioidomycosis is a systemic fungal infection for which a vaccine has been sought for over fifty years. The avirulent Coccidioides posadasii strain, Δcps1 , which is missing a 6 kb gene, showed significant protection in mice. These studies explore conditions of protection in mice and elucidate the immune response. Mice were vaccinated with different doses and viability states of Δcps1 spores, challenged with virulent C. posadasii , and sacrificed at various endpoints, dependent on experimental objectives. Tissues from vaccinated mice were harvested for in vitro elucidation of immune response. Vaccination with viable Δcps1 spores was required for protection from lethal challenge. Viable spore vaccination produced durable immunity, lasting at least 6 months, and prolonged survival (≥6 months). The C. posadasii vaccine strain also protected mice against C. immitis (survival ≥ 6 months). Cytokines from infected lungs of vaccinated mice in the first four days after Cp challenge showed significant increases of IFN-γ, as did stimulated CD4 + spleen cells from vaccinated mice. Transfer of CD4 + cells, but not CD8 + or B cells, reduced fungal burdens following challenge. IFN-γ from CD4 + cells in vaccinated mice indicates a Th1 response, which is critical for host control of coccidioidomycosis. [ABSTRACT FROM AUTHOR]

Qat (Catha edulis, Celastraceae) is a woody evergreen species with great economic and cultural importance. It is cultivated for its stimulant alkaloids cathine and cathinone in East Africa and southwest Arabia. However, genome information, especially DNA sequence resources, for C. edulis are limited, hindering studies regarding interspecific and intraspecific relationships. Herein, the complete chloroplast (cp) genome of Catha edulis is reported. This genome is 157,960 bp in length with 37% GC content and is structurally arranged into two 26,577 bp inverted repeats and two single-copy areas. The size of the small single-copy and the large single-copy regions were 18,491 bp and 86,315 bp, respectively. The C. edulis cp genome consists of 129 coding genes including 37 transfer RNA (tRNA) genes, 8 ribosomal RNA (rRNA) genes, and 84 protein coding genes. For those genes, 112 are single copy genes and 17 genes are duplicated in two inverted regions with seven tRNAs, four rRNAs, and six protein coding genes. The phylogenetic relationships resolved from the cp genome of qat and 32 other species confirms the monophyly of Celastraceae. The cp genomes of C. edulis, Euonymus japonicus and seven Celastraceae species lack the rps16 intron, which indicates an intron loss took place among an ancestor of this family. The cp genome of C. edulis provides a highly valuable genetic resource for further phylogenomic research, barcoding and cp transformation in Celastraceae. [ABSTRACT FROM AUTHOR]

In the present study, we sequenced the entire mitochondrial genome (mitogenome) of Ectropis oblique using PCR amplification and sequencing methods The entire mitogenome is 15,356 bp long, including 13 protein coding genes, 22 transfer RNA (tRNA) genes, two ribosomal RNA (rRNA) genes and A + T rich element. The base composition and gene arrangement are identical to those of other lepidopterans. Of these 37 genes, twenty three are resided on heavy strand, while fourteen located on light strand. The newly sequenced mitogenome displayed a biased Adenine/thymine 84.94% usage versus guanine/cytosine. The AT skewness is 0.030 and the GC skewness is −0.180. Twelve out of 13 PCGs initiated with canonical start codon (ATN), while cox1 started with CGA. The A + T rich element of E. oblique is 363 bp long and contains of many features common to lepidopteran insects, including the ‘ATAGA’ motif, a 22 bp poly (T) stretch and a microsatellite-like (AT) 8 element upstream of trnM . Further, this mitogenome comprises 15 intergenic spacer and overlapping regions. Phylogenetic analyses showed that E. oblique belongs to Geometridae, and that the monophyly of Lepidoptera superfamilies is well supported. [ABSTRACT FROM AUTHOR]

During protein synthesis, the ribosome simultaneously binds up to three different transfer RNA (tRNA) molecules. Among the three tRNA binding sites, the regulatory role of the exit (E) site, where deacylated tRNA spontaneously dissociates from the translational complex, has remained elusive. Here we use two donor--quencher pairs to observe and correlate both the conformation of ribosomes and tRNAs as well as tRNA occupancy. Our results reveal a partially rotated state of the ribosome wherein all three tRNA sites are occupied during translation elongation. The appearance and lifetime of this state depend on the E-site tRNA dissociation kinetics, which may vary among tRNA species and depends on temperature and ionic strength. The 3-tRNA partially rotated state is not a proper substrate for elongation factor G (EF-G), thus inhibiting translocation until the E-site tRNA dissociates. Our result presents two parallel kinetic pathways during translation elongation, underscoring the ability of E-site codons to modulate the dynamics of protein synthesis. [ABSTRACT FROM AUTHOR]

The mitochondrial genome of Mesomelena mesomelaena (Loew, 1848) is the first to be sequenced in the flesh fly subfamily Miltogramminae (Diptera: Sarcophagidae). The 14,559 bp mitogenome contains 37 typical metazoan mitochondrial genes: 13 protein-coding genes, two ribosomal RNA genes and 22 transfer RNA genes, with the same locations as in the insect ground plan. All the protein-coding genes have the start codon ATN, except for cox1 (TCG). Eight protein-coding genes have the stop codon TAA, while the remaining five have the stop codon T (cox1, cox2, nad5, and nad4) or TAG (cytb). Synonymous and non-synonymous substitution rates (Ks and Ka) for each protein-coding gene indicate that these genes evolved primarily under negative (or purifying) selection (Ka < Ks). Phylogeny of Sarcophagidae is proposed based on all the sarcophagid mitogenomes in GenBank, and the subfamily topology is reconstructed as (Sarcophaginae (Paramacronychiinae, Miltogramminae)). [ABSTRACT FROM AUTHOR]

Saccharomyces cerevisiae cells are killed by zymocin, a tRNase ribotoxin complex from Kluyveromyces lactis, which cleaves anticodons and inhibits protein synthesis. Zymocin's action requires specific chemical modification of uridine bases in the anticodon wobble position (U34) by the Elongator complex (Elp1-Elp6). Hence, loss of anticodon modification in mutants lacking Elongator or related KTI (K lactis Toxin Insensitive) genes protects against tRNA cleavage and confers resistance to the toxin. Here, we show that zymocin can be used as a tool to genetically analyse KTI12, a gene previously shown to code for an Elongator partner protein. From a kti12 mutant pool of zymocin survivors, we identify motifs in Kti12 that are functionally directly coupled to Elongator activity. In addition, shared requirement of U34 modifications for nonsense and missense tRNA suppression (SUP4; SOE1) strongly suggests that Kti12 and Elongator cooperate to assure proper tRNA functioning. We show that the Kti12 motifs are conserved in plant ortholog DRL1/ELO4 from Arabidopsis thaliana and seem to be involved in binding of cofactors (e.g., nucleotides, calmodulin). Elongator interaction defects triggered by mutations in these motifs correlate with phenotypes typical for loss of U34 modification. Thus, tRNA modification by Elongator appears to require physical contact with Kti12, and our preliminary data suggest that metabolic signals may affect proper communication between them. [ABSTRACT FROM AUTHOR]

In the present study, the complete sequence of the mitochondrial genome (mitogenome) of Daphnis nerii (Lepidoptera: Sphingidae) is described. The mitogenome (15,247 bp) of D.nerii encodes13 protein-coding genes (PCGs), 22 transfer RNA genes (tRNAs), two ribosomal RNA genes (rRNAs) and an adenine (A) + thymine (T)-rich region. Its gene complement and order is similar to that of other sequenced lepidopterans. The 12 PCGs initiated by ATN codons except for cytochrome c oxidase subunit 1 (cox1) gene that is seemingly initiated by the CGA codon as documented in other insect mitogenomes. Four of the 13 PCGs have the incomplete termination codon T, while the remainder terminated with the canonical stop codon. This mitogenome has six major intergenic spacers, with the exception of A+T-rich region, spanning at least 10 bp. The A+T-rich region is 351 bp long, and contains some conserved regions, including ‘ATAGA’ motif followed by a 17 bp poly-T stretch, a microsatellite-like element (AT)9 and also a poly-A element. Phylogenetic analyses based on 13 PCGs using maximum likelihood (ML) and Bayesian inference (BI) revealed that D. nerii resides in the Sphingidae family. [ABSTRACT FROM AUTHOR]

Strict L-chiral rejection through Gly-cisPro motif during chiral proofreading underlies the inability of D-aminoacyl-tRNA deacylase (DTD) to discriminate between D-amino acids and achiral glycine. The consequent Gly-tRNAGly 'misediting paradox' is resolved by EF-Tu in the cell. Here, we show that DTD's active site architecture can efficiently edit mischarged Gly-tRNAAla species four orders of magnitude more efficiently than even AlaRS, the only ubiquitous cellular checkpoint known for clearing the error. Also, DTD knockout in AlaRS editing-defective background causes pronounced toxicity in Escherichia coli even at low-glycine levels which is alleviated by alanine supplementation. We further demonstrate that DTD positively selects the universally invariant tRNAAla-specific G3• U70. Moreover, DTD's activity on non-cognate Gly-tRNAAla is conserved across all bacteria and eukaryotes, suggesting DTD's key cellular role as a glycine deacylator. Our study thus reveals a hitherto unknown function of DTD in cracking the universal mechanistic dilemma encountered by AlaRS, and its physiological importance. [ABSTRACT FROM AUTHOR]

Eleusine indica , also known as goosegrass, is a serious weed in at least 42 countries. In this paper we report the complete plastid genome sequence of goosegrass obtained by de novo assembly of paired-end and mate-paired reads generated by Illumina sequencing of total genomic DNA. The goosegrass plastome is a circular molecule of 135,151 bp in length, consisting of two single-copy regions separated by a pair of inverted repeats (IRs) of 20,919 bases. The large (LSC) and the small (SSC) single-copy regions span 80,667 bases and 12,646 bases, respectively. The plastome of goosegrass has 38.19% GC content and includes 108 unique genes, of which 76 are protein-coding, 28 are transfer RNA, and 4 are ribosomal RNA. The goosegrass plastome sequence was compared to eight other species of Poaceae. Although generally conserved with respect to Poaceae, this genomic resource will be useful for evolutionary studies within this weed species and the genus Eleusine . [ABSTRACT FROM AUTHOR]

The 20 aminoacyl tRNA synthetases (aaRSs) couple each amino acid to their cognate tRNAs. During evolution, 19 aaRSs expanded by acquiring novel noncatalytic appended domains, which are absent from bacteria and many lower eukaryotes but confer extracellular and nuclear functions in higher organisms. AlaRS is the single exception, with an appended C-terminal domain (C-Ala) that is conserved from prokaryotes to humans but with a wide sequence divergence. In human cells, C-Ala is also a splice variant of AlaRS. Crystal structures of two forms of human C-Ala, and small-angle X-ray scattering of AlaRS, showed that the large sequence divergence of human C-Ala reshaped C-Ala in a way that changed the global architecture of AlaRS. This reshaping removes the role of C-Ala in prokaryotes for docking tRNA and instead repurposes it to form a dimer interface presenting a DNA-binding groove. This groove cannot form with the bacterial ortholog. Direct DNA binding by human C-Ala, but not by bacterial C-Ala, was demonstrated. Thus, instead of acquiring a novel appended domain like other human aaRSs, which engendered novel functions, a new AlaRS architecture was created by diversifying a preexisting appended domain. [ABSTRACT FROM AUTHOR]

Background: While the CCA sequence at the mature 3é end of tRNAs is conserved and critical for translational function, a genetic template for this sequence is not always contained in tRNA genes. In eukaryotes and Archaea, the CCA ends of tRNAs are synthesized post-transcriptionally by CCA-adding enzymes. In Bacteria, tRNA genes template CCA sporadically. Results: In order to understand the variation in how prokaryotic tRNA genes template CCA, we re-annotated tRNA genes in tRNAdb-CE database version 0.8. Among 132,129 prokaryotic tRNA genes, initiator tRNA genes template CCA at the highest average frequency (74.1%) over all functional classes except selenocysteine and pyrrolysine tRNA genes (88.1% and 100% respectively). Across bacterial phyla and a wide range of genome sizes, many lineages exist in which predominantly initiator tRNA genes template CCA. Convergent and parallel retention of CCA templating in initiator tRNA genes evolved in independent histories of reductive genome evolution in Bacteria. Also, in a majority of cyanobacterial and actinobacterial genera, predominantly initiator tRNA genes template CCA. We also found that a surprising fraction of archaeal tRNA genes template CCA. Conclusions: We suggest that cotranscriptional synthesis of initiator tRNA CCA 3é ends can complement inefficient processing of initiator tRNA precursors, "bootstrap" rapid initiation of protein synthesis from a non-growing state, or contribute to an increase in cellular growth rates by reducing overheads of mass and energy to maintain nonfunctional tRNA precursor pools. More generally, CCA templating in structurally non-conforming tRNA genes can afford cells robustness and greater plasticity to respond rapidly to environmental changes and stimuli. [ABSTRACT FROM AUTHOR]

The coevolution theory of the origin of the genetic code maintains that the biosynthetic relationships between amino acids co-evolved with the genetic code organization. In other words, the metabolism of amino acids co-evolved with the organization of the genetic code because the biosynthetic pathways of amino acids occurred on tRNA-like molecules. Thus, a heterotrophic origin of amino acids-also only of those involved in the early phase of the structuring of the genetic code-would seem to contradict the main postulate of the coevolution theory. As a matter of fact, this origin not being linked to the metabolism of amino acids in any way-being taken from a physical setting-would seem to remove the possibility that this metabolism had instead heavily contributed to the structuring of the genetic code. Therefore, I have analyzed the structure of the genetic code and mechanisms that brought to its structuring for understanding if the coevolution theory is compatible with autotrophic or heterotrophic conditions. One of the arguments was that an autotrophic origin of amino acids would have the advantage to be able to directly link their metabolism to the structure of the genetic code if-as hypothesized by the coevolution theory-the biosyntheses of amino acids occurred on tRNA-like molecules. Simultaneously, a heterotrophic origin would not have been able to link the metabolism of amino acids to the structure of the genetic code for the absence of a precise determinism of allocation of amino acids, that is to say of a clear mechanism-linked to tRNA-like molecules, for example-that would have determined the specific pattern observed in the genetic code of the biosynthetic relationships between amino acids. The conclusion is that an autotrophic origin of coded amino acids would seem to be the condition under which the genetic code originated. [ABSTRACT FROM AUTHOR]

Recent evidence indicates that inhibition of protein translation may be a common pathogenic mechanism for peripheral neuropathy associated with mutant tRNA synthetases (aaRSs). aaRSs are enzymes that ligate amino acids to their cognate tRNA, thus catalyzing the first step of translation. Dominant mutations in five distinct aaRSs cause Charcot-Marie-Tooth (CMT) peripheral neuropathy, characterized by length-dependent degeneration of peripheral motor and sensory axons. Surprisingly, loss of aminoacylation activity is not required for mutant aaRSs to cause CMT. Rather, at least for some mutations, a toxic-gain-of-function mechanism underlies CMT-aaRS. Interestingly, several mutations in two distinct aaRSs were recently shown to inhibit global protein translation in Drosophila models of CMT-aaRS, by a mechanism independent of aminoacylation, suggesting inhibition of translation as a common pathogenic mechanism. Future research aimed at elucidating the molecular mechanisms underlying the translation defect induced by CMT-mutant aaRSs should provide novel insight into the molecular pathogenesis of these incurable diseases. [ABSTRACT FROM AUTHOR]

Codon usage bias affects protein translation because tRNAs that recognize synonymous codons differ in their abundance. Although the current dogma states that tRNA expression is exclusively regulated by intrinsic control elements (A- and B-box sequences), we revealed, using a reporter that monitors the levels of individual tRNA genes in Caenorhabditis elegans, that eight tryptophan tRNA genes, 100% identical in sequence, are expressed in different tissues and change their expression dynamically. Furthermore, the expression levels of the sup-7 tRNA gene at day 6 were found to predict the animal’s lifespan. We discovered that the expression of tRNAs that reside within introns of protein-coding genes is affected by the host gene’s promoter. Pairing between specific Pol II genes and the tRNAs that are contained in their introns is most likely adaptive, since a genome-wide analysis revealed that the presence of specific intronic tRNAs within specific orthologous genes is conserved across Caenorhabditis species. [ABSTRACT FROM AUTHOR]

The ability of RNA polymerase (RNAP) III to efficiently recycle from termination to reinitiation is critical for abundant tRNA production during cellular proliferation, development and cancer. Yet understanding of the unique termination mechanisms used by RNAP III is incomplete, as is its link to high transcription output. We used two tRNA-mediated suppression systems to screen for Rpc1 mutants with gain- and loss- of termination phenotypes in S. pombe. 122 point mutation mutants were mapped to a recently solved 3.9 Å structure of yeast RNAP III elongation complex (EC); they cluster in the active center bridge helix and trigger loop, as well as the pore and funnel, the latter of which indicate involvement of the RNA cleavage domain of the C11 subunit in termination. Purified RNAP III from a readthrough (RT) mutant exhibits increased elongation rate. The data strongly support a kinetic coupling model in which elongation rate is inversely related to termination efficiency. The mutants exhibit good correlations of terminator RT in vitro and in vivo, and surprisingly, amounts of transcription in vivo. Because assessing in vivo transcription can be confounded by various parameters, we used a tRNA reporter with a processing defect and a strong terminator. By ruling out differences in RNA decay rates, the data indicate that mutants with the RT phenotype synthesize more RNA than wild type cells, and than can be accounted for by their increased elongation rate. Finally, increased activity by the mutants appears unrelated to the RNAP III repressor, Maf1. The results show that the mobile elements of the RNAP III active center, including C11, are key determinants of termination, and that some of the mutations activate RNAP III for overall transcription. Similar mutations in spontaneous cancer suggest this as an unforeseen mechanism of RNAP III activation in disease. [ABSTRACT FROM AUTHOR]

The maturation of tRNA precursors involves the 5′ cleavage of leader sequences by an essential endonuclease called RNase P. Beyond the ancestral ribonucleoprotein ( RNP) RNase P, a second type of RNase P called PRORP (protein-only RNase P) evolved in eukaryotes. The current view on the distribution of RNase P in cells is that multiple RNPs, multiple PRORPs or a combination of both, perform specialised RNase P activities in the different compartments where gene expression occurs. Here, we identify a single gene encoding PRORP in the green alga Chlamydomonas reinhardtii while no RNP is found. We show that its product, Cr PRORP, is triple-localised to mitochondria, the chloroplast and the nucleus. Its downregulation results in impaired tRNA biogenesis in both organelles and the nucleus. Cr PRORP, as a single-subunit RNase P for an entire organism, makes up the most compact and versatile RNase P machinery described in either prokaryotes or eukaryotes. [ABSTRACT FROM AUTHOR]

Background: TRNT1 (CCA-adding transfer RNA nucleotidyl transferase) enzyme deficiency is a new metabolic disease caused by defective post-transcriptional modification of mitochondrial and cytosolic transfer RNAs (tRNAs).Results: We investigated four patients from two families with infantile-onset cyclical, aseptic febrile episodes with vomiting and diarrhoea, global electrolyte imbalance during these episodes, sideroblastic anaemia, B lymphocyte immunodeficiency, retinitis pigmentosa, hepatosplenomegaly, exocrine pancreatic insufficiency and renal tubulopathy. Other clinical features found in children include sensorineural deafness, cerebellar atrophy, brittle hair, partial villous atrophy and nephrocalcinosis. Whole exome sequencing and bioinformatic filtering were utilised to identify recessive compound heterozygous TRNT1 mutations (missense mutation c.668T>C, p.Ile223Thr and a novel splice mutation c.342+5G>T) segregating with disease in the first family. The second family was found to have a homozygous TRNT1 mutation (c.569G>T), p.Arg190Ile, (previously published). We found normal mitochondrial translation products using passage matched controls and functional perturbation of 3' CCA addition to mitochondrial tRNAs (tRNA(Cys), tRNA(LeuUUR) and tRNA(His)) in fibroblasts from two patients, demonstrating a pathomechanism affecting the CCA addition to mt-tRNAs. Acute management of these patients included transfusion for anaemia, fluid and electrolyte replacement and immunoglobulin therapy. We also describe three-year follow-up findings after treatment by bone marrow transplantation in one patient, with resolution of fever and reversal of the abnormal metabolic profile.Conclusions: Our report highlights that TRNT1 mutations cause a spectrum of disease ranging from a childhood-onset complex disease with manifestations in most organs to an adult-onset isolated retinitis pigmentosa presentation. Systematic review of all TRNT1 cases and mutations reported to date revealed a distinctive phenotypic spectrum and metabolic and other investigative findings, which will facilitate rapid clinical recognition of future cases. [ABSTRACT FROM AUTHOR]

Pathogenic mitochondrial DNA (mtDNA) mutations leading to mitochondrial dysfunction can cause cardiomyopathy and heart failure. These mutations were described in themt-tRNAgenes and in the mitochondrial protein-coding genes. The aim of this study was to identify the genetic defect in two patients belonging to two families with cardiac dysfunction associated to a wide spectrum of clinical phenotypes. The sequencing analysis of the whole mitochondrial DNA in the two patients and their parents revealed the presence of known polymorphisms associated to cardiomyopathy and two pathogenic mutations in DNA extracted from blood leucocytes: the heteroplasmic m.3243A > G mutation in theMT-TL1gene in patient A; and the homoplasmic m.5182C > T mutation in theND2gene in patient B. Secondary structure analysis of the ND2 protein further supported the deleterious role of the m.5182C > T mutation, as it was found to be involved an extended imbalance in its hydrophobicity and affect its function. In addition, the mitochondrial variants identified in patients A and B classify both of them in the same haplogroup H2a2a1. [ABSTRACT FROM AUTHOR]

Elucidating the genomic features influencing prokaryotic growth rates has always been a study of interest. Previously, it was observed that overlapping genes (OGs) play a crucial role in the prokaryotic genome size reduction. This study is focused to explore whether OGs act as a potential correlate of prokaryotic growth rates. For this purpose, we compiled a dataset of 25 archaeal and 117 eubacterial genomes and analyzed the inter-correlation between the proportion of overlapping regions in these genomes with their growth rates. Here, we observed that the proportion of overlapping region holds a significant negative correlation with generation time in archaeal domain, whereas no correlation was observed in the eubacterial domain. However, after masking the effect of tRNA, rRNA multiplicity and environmental diversity, OGs show an independent effect over growth rates in the eubacterial domain as well as in the archaeal domain. Moreover, the influence of OGs on prokaryotic growth rates provides different delineations in archaeal and eubacterial domains. In archaea, both long overlap frequency (LOF) and short overlap frequency (SOF) influence the growth rates by increasing the degree of operonization. On the contrary, in the case of bacteria, neither SOF nor LOF plays any significant role in achieving faster growth rates. [ABSTRACT FROM AUTHOR]

Fitness landscapes describe the genotype-fitness relationship and represent major determinants of evolutionary trajectories. However, the vast genotype space, coupled with the difficulty of measuring fitness, has hindered the empirical determination of fitness landscapes. Combining precise gene replacement and next-generation sequencing, we quantified Darwinian fitness under a high-temperature challenge for more than 65,000 yeast strains, each carrying a unique variant of the single-copy tRNAArg CCU gene at its native genomic location. Approximately 1% of single point mutations in the gene were beneficial and 42% were deleterious. Almost half of all mutation pairs exhibited statistically significant epistasis, which had a strong negative bias, except when the mutations occurred at Watson-Crick paired sites. Fitness was broadly correlated with the predicted fraction of correctly folded transfer RNA (tRNA) molecules, thereby revealing a biophysical basis of the fitness landscape. [ABSTRACT FROM AUTHOR]

Exosomes are secreted nanovesicles that are able to transfer RNA and proteins to target cells. The emerging role of mesenchymal stem cell (MSC) exosomes as promoters of aerobic ATP synthesis restoration in damaged cells, prompted us to assess whether they contain an extramitochondrial aerobic respiration capacity. Exosomes were isolated from culture medium of human MSCs from umbilical cord of =37-wk-old newborns or between 28- to 30-wk-old newborns (i.e., term or preterm infants). Characterization of samples was conducted by cytofluorometry. Oxidative phosphorylation capacity was assessed by Western blot analysis, oximetry, and luminometric and fluorometric analyses. MSC exosomes express functional respiratory complexes I, IV, and V, consuming oxygen. ATP synthesis was only detectable in exosomes from term newborns, suggestive of a specific mechanism that is not completed at an early gestational age. Activities are outward facing and comparable to those detected in mitochondria isolated from term MSCs. MSC exosomes display an unsuspected aerobic respiratory ability independent of whole mitochondria. This may be relevant for their ability to rescue cell bioenergetics. The differential oxidative metabolism of preterm vs. term exosomes sheds new light on the preterm newborn's clinical vulnerability. A reduced ability to repair damaged tissue and an increased capability to cope with anoxic environment for preterm infants can be envisaged. [ABSTRACT FROM AUTHOR]

We have previously proposed that tRNAGly was the first tRNA and glycine was the first amino acid incorporated into the genetic code. The next two amino acids incorporated would have been the other two small hydrophilic amino acids serine and aspartic acid, which occurred through the duplication of the tRNAGly sequence, followed by mutation of its anticodon by single C to U transitionmutations, possibly through spontaneous deamination. Interestingly, however, tRNASer has a different structure than most other tRNAs, possessing a long variable arm; because of this tRNASer is classified as a class II tRNA. Also, serine codons are found not only in the bottom right-hand corner of the genetic code table next to those for glycine and aspartic acid, but also in the top row of the table, next to those for two of the most hydrophobic amino acids, leucine and phenylalanine. In the following, I propose that the class II tRNA structure of tRNASer and the arrangement of serine codons in the genetic code provide clues to the early evolution of tRNA and the genetic code. In addition, I address Di Giulio's recent criticism of our proposal that tRNAGly was the first tRNA, and discuss how early peptides produced from a restricted amino acid alphabet of glycine, serine and aspartic acid might have possessed proteolytic activity, which is possibly important for the early recycling of amino acid monomers. [ABSTRACT FROM AUTHOR]

Silent mutations are being intensively studied. We previously showed that the estrogen receptor alpha Ala87's synonymous polymorphism affects its functional properties. Whereas a link has been clearly established between the effect of silent mutations, tRNA abundance and protein folding in prokaryotes, this connection remains controversial in eukaryotic systems. Although a synonymous polymorphism can affect mRNA structure or the interaction with specific ligands, it seems that the relative frequencies of isoacceptor tRNAs could play a key role in the protein-folding process, possibly through modulation of translation kinetics. Conformational changes could be subtle but enough to cause alterations in solubility, proteolysis profiles, functional parameters or intracellular targeting. Interestingly, recent advances describe dramatic changes in the tRNA population associated with proliferation, differentiation or response to chemical, physical or biological stress. In addition, several reports reveal changes in tRNAs' posttranscriptional modifications in different physiological or pathological conditions. In consequence, since changes in the cell state imply quantitative and/or qualitative changes in the tRNA pool, they could increase the likelihood of protein conformational variants, related to a particular codon usage during translation, with consequences of diverse significance. These observations emphasize the importance of genetic code flexibility in the co-translational protein-folding process. [ABSTRACT FROM AUTHOR]

Mutations in mitochondrial tRNAThr gene were recently reported to be associated with coronary heart disease. These mutations, such as T15889C, G15927A, G15930A and A15951G, were claimed to be pathogenic. To examine whether these mutations contributed to the genetic susceptibility to coronary heart disease, we analyzed the conservation index of these mutations between different species. In particular, reports concerning the role of the G15927A mutation was the most controversial. Therefore, based on the previous and this study, we conducted that mutations in mitochondrial tRNAThr gene may not be associated with coronary heart disease. [ABSTRACT FROM AUTHOR]

Vietnamese patients (106) tentatively diagnosed with encephalomyopathy were screened for the presence of 15 common point mutations in mitochondria using PCR-RFLP. The screened mutations include A3243G, T3271C and T3291C for Mitochondrial Encephalopathy, Lactic Acidosis and Stroke-like episodes (MELAS); A8344G and T8356C for Myoclonus Epilepsy and Rag-Red Fibers (MERRF); G11778A, G3460A and T14484C for Leber's Hereditary Optic Neuropathy (LHON); T8993G/C and T9176G for Leigh syndrome; A1555G for deafness syndrome; G4298A, T10010C, T14728C and T14709C for neuromuscular syndrome. As a result, 6 cases of A3243G (5.7%) and 2 cases of T14727C (3.9%) were found. The 6 cases of A3243G mutation were heteroplasmic at different levels (4.23–80.85%). The T14727C change was discovered for the first time in the MTTE gene encoding for tRNAGluand showed homoplasmy. The T14727C change was probably a mutation because it was further confirmed as vertically inherited from the mother and not the result of isolated polymorphism. [ABSTRACT FROM AUTHOR]

Lysobacter dokdonensis DS-58, belonging to the family Xanthomonadaceae, was isolated from a soil sample in Dokdo, Korea in 2011. Strain DS-58 is the type strain of L. dokdonensis. In this study, we determined the genome sequence to describe the genomic features including annotation information and COG functional categorization. The draft genome sequence consists of 25 contigs totaling 3,274,406 bp (67.24 % G + C) and contains 3,155 protein coding genes, 2 copies of ribosomal RNA operons, and 48 transfer RNA genes. Among the protein coding genes, 75.91 % of the genes were annotated with a putative function and 87.39 % of the genes were assigned to the COG category. In the genome of L. dokdonensis, a large number of genes associated with protein degradation and antibiotic resistance were detected. [ABSTRACT FROM AUTHOR]

Tripsacum dactyloides, known as eastern gamagrass, is used as a donor of valuable traits. It grows naturally in the same region where maize is commercially cultured in the USA and has the ability to hybridize to maize. The wild genotype of eastern gamagrass is threaten by the gene flow from the transgenic maize. The circular genome is 141,050 bp in length and contains 120 genes, including 73 protein-coding genes (PCG), 39 transfer RNA genes (tRNA) and eight ribosomal RNA genes (rRNA). The overall nucleotide composition is: 30.8% A, 19.2% C, 19.3% G, 30.7% T, with a total G + C content of 38.5%. The phylogenetic tree was constructed to explore the taxonomic status ofTripsacum dactyloides, which contributes to phylogenetic studies and further conservation strategies for this species. [ABSTRACT FROM PUBLISHER]

The dicistrovirus intergenic region internal ribosome entry site (IRES) adopts a triple-pseudoknotted RNA structure and occupies the core ribosomal E, P, and A sites to directly recruit the ribosome and initiate translation at a non-AUG codon. A subset of dicistrovirus IRESs directs translation in the 0 and +1 frames to produce the viral structural proteins and a +1 overlapping open reading frame called ORFx, respectively. Here we show that specific mutations of two unpaired adenosines located at the core of the three-helical junction of the honey bee dicistrovirus Israeli acute paralysis virus (IAPV) IRES PKI domain can uncouple 0 and +1 frame translation, suggesting that the structure adopts distinct conformations that contribute to 0 or +1 frame translation. Using a reconstituted translation system, we show that ribosomes assembled on mutant IRESs that direct exclusive 0 or +1 frame translation lack reading frame fidelity. Finally, a nuclear magnetic resonance/small-angle X-ray scattering hybrid approach reveals that the PKI domain of the IAPV IRES adopts an RNA structure that resembles a complete tRNA. The tRNA shape-mimicry enables the viral IRES to gain access to the ribosome tRNA-binding sites and form intermolecular contacts with the ribosome that are necessary for initiating IRES translation in a specific reading frame. [ABSTRACT FROM AUTHOR]

tRNA is the most highly modified class of RNA species, and modifications are found in tRNAs from all organisms that have been examined. Despite their vastly different chemical structures and their presence in different tRNAs, occurring in different locations in tRNA, the biosynthetic pathways of the majority of tRNA modifications include a methylation step(s). Recent discoveries have revealed unprecedented complexity in the modification patterns of tRNA, their regulation and function, suggesting that each modified nucleoside in tRNA may have its own specific function. However, in plants, our knowledge on the role of individual tRNA modifications and how they are regulated is very limited. In a genetic screen designed to identify factors regulating disease resistance and activation of defenses in Arabidopsis, we identified SUPPRESSOR OF CSB3 9 (SCS9). Our results reveal SCS9 encodes a tRNA methyltransferase that mediates the 2´-O-ribose methylation of selected tRNA species in the anticodon loop. These SCS9-mediated tRNA modifications enhance during the course of infection with the bacterial pathogen Pseudomonas syringae DC3000, and lack of such tRNA modification, as observed in scs9 mutants, severely compromise plant immunity against the same pathogen without affecting the salicylic acid (SA) signaling pathway which regulates plant immune responses. Our results support a model that gives importance to the control of certain tRNA modifications for mounting an effective immune response in Arabidopsis, and therefore expands the repertoire of molecular components essential for an efficient disease resistance response. [ABSTRACT FROM AUTHOR]

Polyethylene glycol (PEG) of different lengths was genetically incorporated into the backbone of a polypeptide using stop-anticodon and frameshift anticodon-containing tRNAs, which were acylated with PEG-containing amino acids. [ABSTRACT FROM AUTHOR]

Proteins in the cell are synthesized by a ribosome translating the genetic information encoded on the single-stranded messenger RNA (mRNA). It has been shown that the ribosome can also translate through the duplex region of the mRNA by unwinding the duplex. Here, based on our proposed model of the ribosome translation through the mRNA duplex we study theoretically the distribution of dwell times of the ribosome translation through the mRNA duplex under the effect of a pulling force externally applied to the ends of the mRNA to unzip the duplex. We provide quantitative explanations of the available single molecule experimental data on the distribution of dwell times with both short and long durations, on rescuing of the long paused ribosomes by raising the pulling force to unzip the duplex, on translational arrests induced by the mRNA duplex and Shine-Dalgarno(SD)-like sequence in the mRNA. The functional consequences of the pauses or arrests caused by the mRNA duplex and the SD sequence are discussed and compared with those obtained from other types of pausing, such as those induced by "hungry" codons or interactions of specific sequences in the nascent chain with the ribosomal exit tunnel. [ABSTRACT FROM AUTHOR]

Target identification is highly instructive in defining the biological roles of microRNAs. However, little is known about other small noncoding RNAs; for example, tRNA-derived RNA Fragments (tRFs). Some tRFs exhibit a gene-silencing mechanism distinctly different from that of typical microRNAs. We recently demonstrated that a respiratory syncytial virus (RSV)-induced tRF, called tRF5-GluCTC, promotes RSV replication. RSV is the single most important cause of lower respiratory tract infection in children. By using biochemical screening and bioinformatics analyses, we have identified apolipoprotein E receptor 2 (APOER2) as a target of tRF5-GluCTC. The 3′-portion of tRF5-GluCTC recognizes a target site in the 3′-untranslated region of APOER2 and suppresses its expression. We have also discovered that APOER2 is an anti-RSV protein whose suppression by tRF5-GluCTC promotes RSV replication. Our report represents the first identification of a natural target of a tRF and illustrates how a virus utilizes a host tRF to control a host gene to favor its replication. [ABSTRACT FROM AUTHOR]

Summary Proteins begin to fold as they emerge from translating ribosomes. The kinetics of ribosome transit along a given mRNA can influence nascent chain folding, but the extent to which individual codon translation rates impact proteome integrity remains unknown. Here, we show that slower decoding of discrete codons elicits widespread protein aggregation in vivo. Using ribosome profiling, we find that loss of anticodon wobble uridine (U 34 ) modifications in a subset of tRNAs leads to ribosome pausing at their cognate codons in S. cerevisiae and C. elegans . Cells lacking U 34 modifications exhibit gene expression hallmarks of proteotoxic stress, accumulate aggregates of endogenous proteins, and are severely compromised in clearing stress-induced protein aggregates. Overexpression of hypomodified tRNAs alleviates ribosome pausing, concomitantly restoring protein homeostasis. Our findings demonstrate that modified U 34 is an evolutionarily conserved accelerator of decoding and reveal an unanticipated role for tRNA modifications in maintaining proteome integrity. [ABSTRACT FROM AUTHOR]

The article discusses a study which aims to compare the properties of Thermococcus kodakarensis (T. kodakarensis) ribonuclease P (RNase P) components with Pyrococcus horikoshii (P. horikoshii) RNase P. Topics discussed include the amplification of the genes encoding TkoRpp30 (TK1450) and TkoPop5 (TK1767), characterization of TkoPop5 and TkoRpp30, and structural determination, description and comparison between Tko Rpp30 and TkoPop5.

tRNAs are unique among various RNAs in that they shuttle between the nucleus and the cytoplasm, and their localization is regulated by nutrient conditions. Although nuclear export of tRNAs has been well documented, the import machinery is poorly understood. Here, we identified Ssa2p, a major cytoplasmic Hsp70 in Saccharomyces cerevisiae, as a tRNA-binding protein whose deletion compromises nuclear accumulation of tRNAs upon nutrient starvation. Ssa2p recognizes several structural.

Transcriptional regulation of ribosome and tRNA synthesis plays a central role in determining protein synthetic capacity and is tightly controlled in response to nutrient availability and cellular stress. In Saccharomyces cerevisiae, the regulation of ribosome and tRNA synthesis was recently shown to involve the Cdc-like kinase Kns1 and the GSK-3 kinase Mck1. In this study, we explored additional roles for these conserved kinases in processes connected to the target of rapamycin complex 1 (TORC1). We conducted a synthetic chemical-genetic screen in a kns1Δ mck1Δ strain and identified many novel rapamycin-hypersensitive genes. Gene ontology analysis showed enrichment for TORC1-regulated processes (vesicle-mediated transport, autophagy, and regulation of cell size) and identified new connections to protein complexes including the protein kinase CK2. CK2 is considered to be a constitutively active kinase and in budding yeast, the holoenzyme comprises two regulatory subunits, Ckb1 and Ckb2, and two catalytic subunits, Cka1 and Cka2. We show that Ckb1 is differentially phosphorylated in vivo and that Kns1 mediates this phosphorylation when nutrients are limiting and under all tested stress conditions. We determined that the phosphorylation of Ckb1 does not detectably affect the stability of the CK2 holoenzyme but correlates with the reduced occupancy of Ckb1 on tRNA genes after rapamycin treatment. Thus, the differential occupancy of tRNA genes by CK2 is likely to modulate its activation of RNA polymerase III transcription. Our data suggest that TORC1, via its effector kinase Kns1, may regulate the association of CK2 with some of its substrates by phosphorylating Ckb1. [ABSTRACT FROM AUTHOR]

Elongator is a conserved protein complex comprising six different polypeptides that has been ascribed a wide range of functions, but which is now known to be required for modification of uridine residues in the wobble position of a subset of tRNAs in yeast, plants, worms and mammals. In previous work, we showed that Elongator's largest subunit (Elp1; also known as Iki3) was phosphorylated and implicated the yeast casein kinase I Hrr25 in Elongator function. Here we report identification of nine in vivo phosphorylation sites within Elp1 and show that four of these, clustered close to the Elp1 C-terminus and adjacent to a region that binds tRNA, are important for Elongator's tRNA modification function. Hrr25 protein kinase directly modifies Elp1 on two sites (Ser-1198 and Ser-1202) and through analyzing non-phosphorylatable (alanine) and acidic, phosphomimic substitutions at Ser-1198, Ser-1202 and Ser-1209, we provide evidence that phosphorylation plays a positive role in the tRNA modification function of Elongator and may regulate the interaction of Elongator both with its accessory protein Kti12 and with Hrr25 kinase. [ABSTRACT FROM AUTHOR]

We determined the complete mitochondrial genome (Mitogome) ofCtenopharyngodon idella var. gold grass carp (C. idella var.) (Accession No.:KT894100) and compered it with a previously published mitogenome (Accession No.:NC010288.1) of Chinese common grass carp. The total length of mitogenome is 16 609 bp with 13 protein-coding genes, 2 rRNA genes, 22 tRNA genes and a control region. The nucleotide compositions of the L-strand are 31.87% for A, 26.20% for T, 15.68% for G, 26.26% for C. Most of the protein-coding genes began with an ATG start codon except for COX1 and ND3 gene. The sequence similarity was 99.81% between each other. There were 32 variation loci obtained, including of 23 transitions, 7 transversions and 2 INDELs. [ABSTRACT FROM PUBLISHER]

The complete mitochondrial genome of the Saxaul Sparrow (Passer ammodendri) was 16 782 bp in length. The Genbank accession number was KT895996. And the content of A, T, C, and G were 30.08% (5048 bp), 22.91% (3845 bp), 32.08% (5384 bp), and 14.93% (2505 bp), respectively. It contained 13 protein-coding genes, 2 rRNA genes, 22 tRNA genes, 1 control region and was similar to most of the other Passeridae birds in gene arrangement and composition. All protein-coding genes used the typical initiation codon ATG, except GTG forCOIand ATA forND3which was the same to the Tree Sparrow (Passer montanus) but different from the House Sparrow (Passer domestic). Most of the stop codons were consistent with the Tree Sparrow and the House Sparrow except forND1,ND3, andND6genes, which were terminated with AGG, TAA, and TAG codons, respectively. Besides, the phylogenetic relationship of Passeriformes based on complete mitochondrial genomes showed that the genetic distance among Passeridae, Emberizidae, and Fringillidae was closer than the others. [ABSTRACT FROM PUBLISHER]

In this study, we report the complete mitochondrial genome of the Greater Mouse-Eared Bat,Myotis myotis.The mitogenome is 17 213 bp with base composition A (34.2%), G (13%), C (22.4%), and T (30.5%). The genome shows conserved synteny with other mammalian mitogenomes, containing 13 protein-coding genes, 2 ribosomal RNA genes, 22 transfer RNA genes, and 1 control region (D-Loop). The majority of the genes are encoded on the H-Strand, except forND6and eight tRNAs. All protein-coding genes start with the ATG start codon, except forND2,ND3,andND5which begin with ATT or ATA. Seven protein-coding genes terminated in a canonical stop codon, TAA or TAG, five contain incomplete stop codons, T or TA.Cytochrome bterminates in the mitochondria specific stop codon AGA. This mitogenome provides a valuable resource for future studies ofM. myotisand other bat and mammal species. [ABSTRACT FROM PUBLISHER]

The mitochondrial genome (mitogenome) ofMegachile sculpturalis(Hymenoptera: Megachilidae) has been reported in this study. This is the first sequenced mitogenome from the family Megachilidae. The sequenced region of this mitochondrial genome is determined to be 16 581 bp in length, including 13 protein-coding genes, 2 ribosomal RNAs, 22 transfer RNAs, and a partial sequence of the AT-rich region, and the AT-rich region contains several characteristic repeated sequences. Additionally, we conducted a phylogenetic analysis using all the mitochondrial genomes of Apoidea that are available in Genbank. Bayesian method supported the monophyly of both Apidae and Colletidae. And Megachilidae was inferred as the sister group of Apidae. [ABSTRACT FROM PUBLISHER]

The complete mitochondrial genome sequence of the serpent mudskipperParapocryptes serperasterwas first determined in this study. The circle genome was 17 243 bp long and consisted of 13 protein-coding genes, 2 rRNA genes, 22 tRNA genes, and 1 control region. The nucleotide composition of the heavy strand ofP. serperasteris 28.65% for A, 30.07% for C, 25.31% for T, and 15.97% for G, with a slight A + T bias of 53.96%. Only the NADH dehydrogenase subunit 6 (ND6) and eight tRNA genes were encoded on the light strand, all other mitochondrial genes were encoded on the heavy strand. A 178-bp tandem repeat, which started from the 827-bp site of the control region, was identified. Like most other gobies,P. serperasteralso has the typical vertebrate mitochondrial gene arrangement. The phylogenetic analysis showed that the kinship betweenParapocryptesandBoleophthalmusis closer than those betweenParapocryptesand other selected genera. [ABSTRACT FROM PUBLISHER]

Claea dabryi is a small bottom-dwelling fish that is endemic to the upper stream of the Yangtze River. In this study, we successfully sequenced the first mitochondrial genome of C. dabryi. The mitogenome is 16 569 bp in length, containing 13 protein-coding genes, 2 rRNA genes, 22 tRNA genes, and a control region (D-loop). Most of the genes are encoded on the heavy strand, except for eight tRNAs (tRNAGln, tRNAAla, tRNAAsn, tRNACys, tRNATyr, tRNASer, tRNAGlu, and tRNAPro) and ND6 gene. In this paper, we utilized 12 protein-coding genes of C. dabryi and other 11 closely species to construct the species phylogenetic tree to verify the accuracy of C. dabryi. [ABSTRACT FROM AUTHOR]