Evolutionary change within a bipotential switch shaped the sperm/oocyte decision in hermaphroditic nematodes.
Evolutionary change within a bipotential switch shaped the sperm/oocyte decision in hermaphroditic nematodes.
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DOI：
10.1371/journal.pgen.1003850
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发表时间：
2013
期刊：
影响因子：
4.5
通讯作者：
Ellis RE
中科院分区：
文献类型：
--
作者：
Guo Y;Chen X;Ellis RE
转录因子的一个子集，如Gli 2和Oct 1是双能的-它们可以激活或抑制相同的目标，以响应来自上游基因的变化信号。以前的一些研究表明，性别决定蛋白TRA-1也可能是双电位的;在这里，我们通过确定一个辅助因子来证实这一假设，并用它来探索双电位开关的结构在进化过程中如何变化。首先，无效突变体揭示了C。Briggsae TRR-1是精子发生所需的，RNA干扰意味着它作为Tip 60组蛋白乙酰转移酶复合物的一部分起作用，RT-PCR数据显示它促进精子发生所需的基因Cbr-fog-3的表达。第二，上位性测试表明TRR-1通过TRA-1起作用，既激活Cbr-fog-3又控制精子/卵母细胞的决定。由于先前的研究表明TRA-1也可以抑制fog-3，这些观察表明它是双电位的。第三，TRR-1还调节雄性尾巴的发育。由于Cbr-tra-2 Cbr-trr-1双突变体类似于Cbr-tra-1无效突变体，这两个调节分支控制所有tra-1活性。第四，在最近的进化过程中，开关的这两个分支之间的关系出现了显著的差异。C. Briggsae trr-1无效突变体阻止雌雄同体精子发生，但不能阻止破坏另一半开关的Cbr-fem无效突变体。另一方面，C. elegans fem null突变体阻止精子发生，但Cel-trr-1突变体不阻止精子发生。然而，合成的相互作用证实了开关的两个半部分存在于每个物种中。因此，在进化过程中，双电位开关的两个部分之间的关系可以迅速改变，因此相同的表型是由替代的互补机制产生的。在蛔虫中，转录因子TRA-1控制性发育。我们表明，TRR-1是一个复杂的蛋白质的一部分，增加了乙酰基的目标，这个复杂的工程与TRA-1启动精子发生。相反，TRA-1的截短形式阻断精子发生。由于该转录因子的两种不同形式相互对立，因此TRA-1是双能的。为了了解这两种形式之间的相互依赖关系是否影响了进化变化，我们比较了相关的蛔虫物种。在一个物种中，影响TRR-1的突变会导致所有生殖细胞变成卵母细胞，但影响三种FEM蛋白（也调节TRA-1）的突变则不会。在其他物种中，这些调控基因的作用是颠倒的。因此，在最近的进化过程中，这种双电位开关的两个半部分的相对重要性发生了变化。
A subset of transcription factors like Gli2 and Oct1 are bipotential — they can activate or repress the same target, in response to changing signals from upstream genes. Some previous studies implied that the sex-determination protein TRA-1 might also be bipotential; here we confirm this hypothesis by identifying a co-factor, and use it to explore how the structure of a bipotential switch changes during evolution. First, null mutants reveal that C. briggsae TRR-1 is required for spermatogenesis, RNA interference implies that it works as part of the Tip60 Histone Acetyl Transferase complex, and RT-PCR data show that it promotes the expression of Cbr-fog-3, a gene needed for spermatogenesis. Second, epistasis tests reveal that TRR-1 works through TRA-1, both to activate Cbr-fog-3 and to control the sperm/oocyte decision. Since previous studies showed that TRA-1 can repress fog-3 as well, these observations demonstrate that it is bipotential. Third, TRR-1 also regulates the development of the male tail. Since Cbr-tra-2 Cbr-trr-1 double mutants resemble Cbr-tra-1 null mutants, these two regulatory branches control all tra-1 activity. Fourth, striking differences in the relationship between these two branches of the switch have arisen during recent evolution. C. briggsae trr-1 null mutants prevent hermaphrodite spermatogenesis, but not Cbr-fem null mutants, which disrupt the other half of the switch. On the other hand, C. elegans fem null mutants prevent spermatogenesis, but not Cel-trr-1 mutants. However, synthetic interactions confirm that both halves of the switch exist in each species. Thus, the relationship between the two halves of a bipotential switch can shift rapidly during evolution, so that the same phenotype is produce by alternative, complementary mechanisms. In roundworms, the transcription factor TRA-1 controls sexual development. We show that TRR-1 is part of a complex of proteins that adds acetyl groups to its targets, and that this complex works with TRA-1 to initiate spermatogenesis. By contrast, a truncated form of TRA-1 blocks spermatogenesis. Because two different forms of this transcription factor oppose each other, TRA-1 is bipotential. To see if the interdependent relationship between these two forms has affected evolutionary change, we compared related species of roundworms. In one species, mutations that affect TRR-1 cause all germ cells to become oocytes, but mutations that affect three FEM proteins, which also regulate TRA-1, do not. In the other species, the roles of these regulatory genes are reversed. Thus, the relative importance of the two halves of this bipotential switch has changed during recent evolution.
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影响因子：
11.8
作者：
Ceol, CJ;Horvitz, HR
通讯作者：
Horvitz, HR
DOI：
10.1073/pnas.1108068108
发表时间：
2011-12-06
影响因子：
11.1
作者：
Beadell, Alana V.;Liu, Qinwen;Haag, Eric S.
通讯作者：
Haag, Eric S.
影响因子：
11.8
作者：
Hill, RC;de Carvalho, CE;Haag, ES
通讯作者：
Haag, ES
影响因子：
9.8
作者：
Duveau F;Félix MA
通讯作者：
Félix MA
影响因子：
10.5
作者：
HODGKIN, J
通讯作者：
HODGKIN, J