The embryonic mir-35 family of microRNAs promotes multiple aspects of fecundity in Caenorhabditis elegans.

The embryonic mir-35 family of microRNAs promotes multiple aspects of fecundity in Caenorhabditis elegans.
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DOI:
10.1534/g3.114.011973
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发表时间:
2014-07-21
期刊:
G3 (Bethesda, Md.)
影响因子:
--
通讯作者:
Ambros V
Ambros V
中科院分区:
其他
文献类型:
--
作者:
McJunkin K;Ambros V

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MicroRNA指导所有后生动物物种发育的许多方面。通常,microRNA在特定的发育阶段表达,以执行时间定义的功能。梭秀丽线虫mir-35-42 microRNA在卵母细胞和早期胚胎中大量表达,并且对于胚胎发育是必需的。在这里,我们发现这些胚胎microRNA也令人惊讶地发挥作用,以控制成年雌雄同体产生的后代的数量。使用温度敏感的米尔-35-42家族突变体(米尔-35-41簇的缺失),我们证明了雌雄同体生殖力的三个明显缺陷。在允许的温度下,轻微的精子缺陷会部分降低雌雄同体的生育力。在限制性温度下,体细胞性腺功能障碍与严重的精子缺陷相结合,大大降低了生育力。包括胚胎温度敏感期晚期在内的多条证据支持mir-35-41在发育早期促进后期幼虫精子产生的作用。我们进一步表明,预测的mir-35家族靶点sup-26(抑制因子-26)在此过程中作用于mir-35-41的下游,这表明在mir-35-41缺失突变体中sup-26的去抑制可能有助于温度敏感性的繁殖力丧失。此外,这些microRNA在男性生育力中发挥作用,促进男性特定交配结构的正确形态发生。总的来说,我们的研究结果表明,mir-35-42家族microRNA的强大活性不仅对在一系列温度下的胚胎发育至关重要,而且还使蠕虫能够随后发展完全的生殖能力。
MicroRNAs guide many aspects of development in all metazoan species. Frequently, microRNAs are expressed during a specific developmental stage to perform a temporally defined function. The C. elegans mir-35-42 microRNAs are expressed abundantly in oocytes and early embryos and are essential for embryonic development. Here, we show that these embryonic microRNAs surprisingly also function to control the number of progeny produced by adult hermaphrodites. Using a temperature-sensitive mir-35-42 family mutant (a deletion of the mir-35-41 cluster), we demonstrate three distinct defects in hermaphrodite fecundity. At permissive temperatures, a mild sperm defect partially reduces hermaphrodite fecundity. At restrictive temperatures, somatic gonad dysfunction combined with a severe sperm defect sharply reduces fecundity. Multiple lines of evidence, including a late embryonic temperature-sensitive period, support a role for mir-35-41 early during development to promote subsequent sperm production in later larval stages. We further show that the predicted mir-35 family target sup-26 (suppressor-26) acts downstream of mir-35-41 in this process, suggesting that sup-26 de-repression in mir-35-41 deletion mutants may contribute to temperature-sensitive loss of fecundity. In addition, these microRNAs play a role in male fertility, promoting proper morphogenesis of male-specific mating structures. Overall, our results demonstrate that robust activity of the mir-35-42 family microRNAs not only is essential for embryonic development across a range of temperatures but also enables the worm to subsequently develop full reproductive capacity.
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