The C. elegans Spalt-like protein SEM-4 functions through the SoxC transcription factor SEM-2 to promote a proliferative blast cell fate in the postembryonic mesoderm.

The C. elegans Spalt-like protein SEM-4 functions through the SoxC transcription factor SEM-2 to promote a proliferative blast cell fate in the postembryonic mesoderm.
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DOI:
10.1016/j.ydbio.2017.06.011
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发表时间:
2017-09-01
影响因子:
2.7
通讯作者:
Liu J
Liu J
中科院分区:
生物学3区
文献类型:
--
作者:
Shen Q;Shi H;Tian C;Ghai V;Liu J

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多细胞生物体的正常发育依赖于细胞命运特化、细胞增殖和细胞分化的良好协调调节。梭线虫胚后中胚层提供了一个有用的系统,揭示参与这些过程的因素,并进一步解剖它们的调控关系。已知含有蛋白SEM-4/萨尔的单个Spalt样锌指参与指定增殖性成肌细胞(SM)的命运。我们已经发现SEM-4/萨尔足以促进SM的命运,并且它以细胞自主的方式这样做。我们进一步表明SEM-4/萨尔通过SoxC转录因子SEM-2起作用以促进SM命运。已知SEM-2通过抑制两种BWM特异性转录因子的表达来促进SM命运。鉴于最近在哺乳动物中的发现显示SEM-4的哺乳动物同源物之一Sall 4通过抑制分化而有助于多能性调节,我们的工作表明SEM-4/萨尔蛋白在调节多能性与分化中的功能似乎是进化保守的。
Proper development of a multicellular organism relies on well-coordinated regulation of cell fate specification, cell proliferation and cell differentiation. The C. elegans postembryonic mesoderm provides a useful system for uncovering factors involved in these processes and for further dissecting their regulatory relationships. The single Spalt-like zinc finger containing protein SEM-4/SALL is known to be involved in specifying the proliferative sex myoblast (SM) fate. We have found that SEM-4/SALL is sufficient to promote the SM fate and that it does so in a cell autonomous manner. We further showed that SEM-4/SALL acts through the SoxC transcription factor SEM-2 to promote the SM fate. SEM-2 is known to promote the SM fate by inhibiting the expression of two BWM-specifying transcription factors. In light of recent findings in mammals showing that Sall4, one of the mammalian homologs of SEM-4, contributes to pluripotency regulation by inhibiting differentiation, our work suggests that the function of SEM-4/SALL proteins in regulating pluripotency versus differentiation appears to be evolutionarily conserved.
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