In multicellular organisms, germ cell formation and differentiation are essential for gamete formation and propagation of genomic information to the next generation. Regulation of mature oocyte size is essential for precisely regulating the chromosome segregation. Therefore, this regulation play an essential role in lineage segregation by precisely regulating cell division. At present, the oocyte size regulatory mechanism is not fully understood. Histone modifying enzymes positively and negatively regulate gene expression by modulating nucleosome structure. Among them histone deacetylases (HADCs) limit transcriptionally active regions by inhibiting transcription factor-mediated gene expression. HDACs are divided into four classes (Class I ~ Class IV). Among the four members of Class I, HDAC-1 and HDAC-2 act redundantly to regulate cell survival in mammals. By contrast, C. elegans has three Class I HDACs, HDA-1, HDA-2 and HDA-3. Embryos exposed to
hda-1 (RNAi) exhibit fully penetrant embryonic lethality. However, the functional role of these HDACs in germ cell development has not been explored. In this study, we analyzed the role of HDACs in oocyte size regulation and embryonic development. We analyzed oocyte size by calculating the area of its central cross section, and found that this parameter's variance in
hda-2 (
ok1479) mutants was significantly larger than in wild-type animals. By contrast, an increase in oocyte size variance was not observed in
hda-3 (
ok1991) mutants, or control (RNAi) or
hda-1 (RNAi) treated animals. Embryonic lethalities in
hda-2 (
ok1479) mutants,
hda-3 (
ok1991) mutants, and wild-type animals were 25.5%, 5.5%, and 4.6%, respectively. Finally, introduction of an extrachromosomal array including a GFP::
hda-2 genomic fragment controlled by an ~6.8 kbp
hda-2 5' cis regulatory region rescued oocyte size and embryonic lethality phenotypes. Taken together, these results suggest that among the three Class I HDACs, only
hda-2 is involved in regulating oocyte size and embryogenesis. The embryonic lethality caused by
hda-1 (RNAi) does not correlate with oocyte size variance. We plan to perform phenotypic analyses of the effect of GFP::
hda-2-overexpression and tissue-specific roles for HDA-2 to elucidate its mechanism of oocyte size regulation that impacts embryonic survival and development.