Identification of messenger RNA substrates for mouse T-STAR

Zhang, L. Y.; Zeng, Mei; Chen, P.; Sun, Hua Qin; Tao, Da Chang; Liu, Y. Q.; Lin, Li-Hsiung; Yang, Yuan; Zhang, S. Z.; X., Y.

doi:10.1134/s0006297909110145

Cited by 3 publications

(2 citation statements)

References 28 publications

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“…We also looked at two other exons which are spliced in the testis and which we independently characterised as being regulated by Tra2β. Minigene experiments indicated both the Crebγ and Fabp9 exons [38], [39] were moderately activated by Tra2β, and were also co-ordinately moderately repressed by the Tra2βΔRS1 isoform (Figure 3I and 3J, lanes 1 and 4). Taken together these data are consistent with full length Tra2β protein activating specific target exons, and the Tra2βΔRS1 protein isoform specifically repressing exons which are at least moderately to strongly activated by full length Tra2β, but not acting as a general repressor of cellular splicing.…”

Section: Resultsmentioning

confidence: 99%

Identification of Evolutionarily Conserved Exons as Regulated Targets for the Splicing Activator Tra2β in Development

et al. 2011

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Alternative splicing amplifies the information content of the genome, creating multiple mRNA isoforms from single genes. The evolutionarily conserved splicing activator Tra2β (Sfrs10) is essential for mouse embryogenesis and implicated in spermatogenesis. Here we find that Tra2β is up-regulated as the mitotic stem cell containing population of male germ cells differentiate into meiotic and post-meiotic cells. Using CLIP coupled to deep sequencing, we found that Tra2β binds a high frequency of exons and identified specific G/A rich motifs as frequent targets. Significantly, for the first time we have analysed the splicing effect of Sfrs10 depletion in vivo by generating a conditional neuronal-specific Sfrs10 knock-out mouse (Sfrs10fl/fl; Nestin-Cretg/+). This mouse has defects in brain development and allowed correlation of genuine physiologically Tra2β regulated exons. These belonged to a novel class which were longer than average size and importantly needed multiple cooperative Tra2β binding sites for efficient splicing activation, thus explaining the observed splicing defects in the knockout mice. Regulated exons included a cassette exon which produces a meiotic isoform of the Nasp histone chaperone that helps monitor DNA double-strand breaks. We also found a previously uncharacterised poison exon identifying a new pathway of feedback control between vertebrate Tra2 proteins. Both Nasp-T and the Tra2a poison exon are evolutionarily conserved, suggesting they might control fundamental developmental processes. Tra2β protein isoforms lacking the RRM were able to activate specific target exons indicating an additional functional role as a splicing co-activator. Significantly the N-terminal RS1 domain conserved between flies and humans was essential for the splicing activator function of Tra2β. Versions of Tra2β lacking this N-terminal RS1 domain potently repressed the same target exons activated by full-length Tra2β protein.

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Section: Resultsmentioning

confidence: 99%

Identification of Evolutionarily Conserved Exons as Regulated Targets for the Splicing Activator Tra2β in Development

et al. 2011

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“…In vertebrates, there are three members of KHDRBS, KHDRBS1 (also called Sam68), KHDRBS2 (also called SLM1), and KHDRBS3 (also called SLM2) which share many features such as RNA binding and signal transduction. Interestingly, khdrbs1 knockout mice showed impaired fertility in males as a result of mRNA translational regulation defect during spermiogenesis ( Paronetto et al, 2009 ; Ehrmann and Elliott, 2010 ; Frisone et al, 2015 ), and KHDRBS3 was also involved in spermatogenesis via directly binding to the genes essential for male gametogenesis ( Zhang et al, 2009 ). This function of KHDRBS1 and KHDRBS3 in mice is apparently analogous to their invertebrate orthologs GLD-1 and NSR in term of regulation of gametogenesis.…”

Section: Introductionmentioning

confidence: 99%

Evolutionary and Expression Analyses Show Co-option of khdrbs Genes for Origin of Vertebrate Brain

Yang

Wang

et al. 2018

Front. Genet.

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Genes generated by whole genome duplications (WGD) can be co-opted by changing their regulation process or altering their coding proteins, which has been shown contributable to the emergence of vertebrate morphological novelties such as vertebrate cartilage. Mouse khdrbs genes, differing from its invertebrate orthologs, were mainly expressed in brain, hinting that khdrbs gene family as a member of genetic toolkit may be linked to vertebrate brain development. However, the evolutionary relationship between khdrbs gene family and vertebrate brain development is unclear. First, we analyzed the evolutionary history of khdrbs gene family in metazoans, and then investigated their expression patterns during early development and in adulthood of zebrafish. We found that the duplication of khdrbs gene family by WGD took place in zebrafish, and all zebrafish khdrbs genes were predominantly expressed in the substructures of brain during early development. Given the expression of invertebrate khdrbs gene in germ line, the distinct expression domains of zebrafish khdrbs genes in brain suggested that the duplicated khdrbs genes are co-opted for promoting the evolutionary origin of vertebrate brain.

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L-carnitine extenuates endocrine disruption, inflammatory burst and oxidative stress in carbendazim-challenged male rats via upregulation of testicular StAR and FABP9, and downregulation of P38-MAPK pathways

Salem¹,

Ismail

Zaki

et al. 2021

Toxicology

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Identification of messenger RNA substrates for mouse T-STAR

Cited by 3 publications

References 28 publications

Identification of Evolutionarily Conserved Exons as Regulated Targets for the Splicing Activator Tra2β in Development

Identification of Evolutionarily Conserved Exons as Regulated Targets for the Splicing Activator Tra2β in Development

Evolutionary and Expression Analyses Show Co-option of khdrbs Genes for Origin of Vertebrate Brain

L-carnitine extenuates endocrine disruption, inflammatory burst and oxidative stress in carbendazim-challenged male rats via upregulation of testicular StAR and FABP9, and downregulation of P38-MAPK pathways

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