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General Comment |
Kim M, et al 2002 reported the expression pattern of HSP25 in mouse preimplantation embryo:
Heat shock responses during oocyte maturation.
Heat shock proteins (HSPs) are known to play an important role not only in various
stress conditions such as exposure to heat shock, but also in normal development
and/or differentiation. The role of small heat shock proteins such as HSP25 in early
embryo development remains largely unknown. Reverse transcription-polymerase chain reaction (RT-PCR)
showed that hsp25 mRNA was detected in unfertilized eggs. Hsp25 mRNA was
induced by zygotic gene activation at 2-cell stage, decreased slightly at 4-cell, and
re-increased at morula, with the highest level at blastocyst stage. Interestingly, another
form of hsp25 variant of which 156 bp (52 a.a.) was truncated within the exon1 region
was observed in all stages of preimplantation embryos.grovary HSP25
was detected in the cytoplasm under normal developmental condition. While acute
heat shock (at 43 degrees C for 30 min) caused no significant changes in the
sub-cellular localization of HSP25 in the developing mouse embryos, chronic heat
shock (at 43 degrees C for 3 hr) resulted in a denser immunostaining of HSP25 in the
nucleus than in the cytoplasm, indicating a nuclear translocation of HSP25 by heat
shock. As hsp25 mRNA was detected in the unfertilized egg as a maternal transcript,
we examined the expression of hsp25 mRNA with RT-PCR during oocyte maturation
under normal and heat shock conditions. Hsp25 mRNA was detected at GV (germinal
vesicle)-, GVBD (germinal vesicle breakdown)-, and MII (metaphase II)-oocytes.
The expression of hsp25 mRNA was increased markedly by both acute (for 30 min
and 1 hr) and chronic (for 4 hr) heat shock, but returned to the basal level during
recovery from heat shock in a time-dependent manner, suggesting a thermo-protective
role of HSP25. In contrast to preimplantation embryos, HSP25 was detected both in
the cytoplasm and the nucleus except for the nucleolus, and the cellular localization
was not altered by heat shock. When GV-oocytes were exposed to acute heat shock (at 43 degrees
C for 15 min to 1 hr), they underwent the GVBD and the PB (polar body) emission
successfully. However, under more stringent heat shock conditions (at 43 degrees C
for 2-4 hr), most oocytes were arrested at the GV-stage, and the first PB was not
developed, indicating that chronic heat shock might be inhibitory to the mouse oocyte
maturation. Taken together, these findings suggest that HSP25 is important for mouse
preimplantation embryo development and oocyte maturation.
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