首页> 外文期刊>Developmental dynamics: an official publication of the American Association of Anatomists >TEG-1 CD2BP2 regulates stem cell proliferation and sex determination in the C. elegans germ line and physically interacts with the UAF-1 U2AF65 splicing factor.
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TEG-1 CD2BP2 regulates stem cell proliferation and sex determination in the C. elegans germ line and physically interacts with the UAF-1 U2AF65 splicing factor.

机译:TEG-1 CD2BP2调节线虫种系中的干细胞增殖和性别决定,并与UAF-1 U2AF65剪接因子发生物理相互作用。

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摘要

For a stem cell population to exist over an extended period, a balance must be maintained between self-renewing (proliferating) and differentiating daughter cells. Within the Caenorhabditis elegans germ line, this balance is controlled by a genetic regulatory pathway, which includes the canonical Notch signaling pathway.Genetic screens identified the gene teg-1 as being involved in regulating the proliferation versus differentiation decision in the C. elegans germ line. Cloning of TEG-1 revealed that it is a homolog of mammalian CD2BP2, which has been implicated in a number of cellular processes, including in U4/U6.U5 tri-snRNP formation in the pre-mRNA splicing reaction. The position of teg-1 in the genetic pathway regulating the proliferation versus differentiation decision, its single mutant phenotype, and its enrichment in nuclei, all suggest TEG-1 also functions as a splicing factor. TEG-1, as well as its human homolog, CD2BP2, directly bind to UAF-1 U2AF65, a component of the U2 auxiliary factor.TEG-1 functions as a splicing factor and acts to regulate the proliferation versus meiosis decision. The interaction of TEG-1 CD2BP2 with UAF-1 U2AF65, combined with its previously described function in U4/U6.U5 tri-snRNP, suggests that TEG-1 CD2BP2 functions in two distinct locations in the splicing cascade.
机译:为了使干细胞种群长期存在,必须在自我更新(增殖)和分化子细胞之间保持平衡。在秀丽隐杆线虫种系中,这种平衡受遗传调控途径控制,其中包括经典的Notch信号通路。基因筛查确定teg-1基因参与了秀丽隐杆线虫种系的增殖与分化决定。 。 TEG-1的克隆表明它是哺乳动物CD2BP2的同源物,已与许多细胞过程有关,包括在mRNA剪接前的U4 / U6.U5 tri-snRNP形成中。 teg-1在调控增殖与分化决定的遗传途径中的位置,其单一突变表型及其在细胞核中的富集,均表明TEG-1还可作为剪接因子。 TEG-1及其人类同源物CD2BP2直接与U2辅助因子UAF-1 U2AF65结合.TEG-1作为剪接因子并调节增殖与减数分裂的决定。 TEG-1 CD2BP2与UAF-1 U2AF65的相互作用,结合其先前在U4 / U6.U5 tri-snRNP中的功能,表明TEG-1 CD2BP2在剪接级联的两个不同位置起作用。

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