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논문 기본 정보

자료유형
학술저널
저자정보
Unno Takuma (Ritsumeikan University Japan) Takatsuka Hisashi (Ritsumeikan University Japan) Ohnishi Yuto (Ritsumeikan University Japan) Ito Masahiro (Ritsumeikan University Japan) Kubota Yukihiko (Ritsumeikan University Japan)
저널정보
한국유전학회 Genes & Genomics Genes & Genomics Vol.44 No.3
발행연도
2022.3
수록면
343 - 357 (15page)
DOI
10.1007/s13258-021-01195-9

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Background Caenorhabditis elegans encodes three class I histone deacetylases (HDACs), HDA-1, HDA-2, and HDA-3. Although HDA-1 is known to be involved in embryogenesis, the regulatory roles of HDA-2 and HDA-3 in embryonic development remain unexplored. Objective To elucidate the functional roles of the three class I HDACs in C. elegans embryonic development. Methods The roles of Class I HDACs, HDA-1, HDA-2, and HDA-3 in Caenorhabditis elegans during embryogenesis were investigated through the analysis of embryonic lethality via gene knockdown or deletion mutants. Additionally, the size of these knockdown and mutant eggs was observed using a differential interference contrast microscope. Finally, expression pattern and tissue-specific role of hda-2 and transcriptome of the hda-2 mutant were analyzed. Results Here, we report that HDA-1 and HDA-2, but not HDA-3, play essential roles in Caenorhabditis elegans embryonic development. Our observations of the fertilized egg size variance demonstrated that HDA-2 is involved in regulating the size of fertilized eggs. Combined analysis of expression patterns and sheath cell-specific rescue experiments indicated that the transgenerational role of HDA-2 is involved in the viability of embryonic development and fertilized egg size regulation. Furthermore, transcriptome analysis of hda-2 mutant embryos implies that HDA-2 is involved in epigenetic regulation of embryonic biological processes by downregulating and upregulating the gene expression. Conclusion Our finding suggests that HDA-2 regulates the embryonic development in Caenorhabditis elegans by controling a specific subset of genes, and this function might be mediated by transgenerational epigenetic effect.

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