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<p>The egg cytoplasm undergoes large-scale remodeling after fertilization. Here, we reveal that the germ granule component, HERD-1, is involved in selective degradation of maternal plasma membrane proteins after fertilization in <i>Caenorhabditis elegans</i>. HERD-1 is specifically expressed in the germline and mainly localized in a subtype of germ granules, Z granules. HERD-1 loss caused maternal plasma membrane protein accumulation in ubiquitin-positive early and late endosomal assemblies in the early embryos. The proteomic analysis showed that HERD-1 loss substantially reduced the protein levels of a subset of endolysosomal regulators such as ESCRT-0 components regulating the multivesicular body pathway. Defects in maternal membrane protein degradation in <i>herd-1</i>-deficient embryos were suppressed with the loss of DEPS-1 or PRG-1, which are required for germ granule organization and small-RNA biogenesis. These results suggest that several germ granule components maintain appropriate endolysosomal component levels via small RNA-mediated regulation during the oocyte-to-embryo transition, promoting endosomal switching toward embryogenesis.</p>

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Germ granule components regulate endosomal switching during the oocyte-to-embryo transition in Caenorhabditis elegans

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月7日

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  • Shun-ichi Suto,
  • Koh-ichi Teraoka,
  • Ichiro Kawasaki,
  • Kenta Sugiura,
  • Taeko Sasaki,
  • Ikuko Maejima,
  • Hidetaka Kosako,
  • Miyuki Sato,
  • Ken Sato

摘要

The egg cytoplasm undergoes large-scale remodeling after fertilization. Here, we reveal that the germ granule component, HERD-1, is involved in selective degradation of maternal plasma membrane proteins after fertilization in Caenorhabditis elegans. HERD-1 is specifically expressed in the germline and mainly localized in a subtype of germ granules, Z granules. HERD-1 loss caused maternal plasma membrane protein accumulation in ubiquitin-positive early and late endosomal assemblies in the early embryos. The proteomic analysis showed that HERD-1 loss substantially reduced the protein levels of a subset of endolysosomal regulators such as ESCRT-0 components regulating the multivesicular body pathway. Defects in maternal membrane protein degradation in herd-1-deficient embryos were suppressed with the loss of DEPS-1 or PRG-1, which are required for germ granule organization and small-RNA biogenesis. These results suggest that several germ granule components maintain appropriate endolysosomal component levels via small RNA-mediated regulation during the oocyte-to-embryo transition, promoting endosomal switching toward embryogenesis.