Analysis On The Cause Of Embryonic Lethality In RBBP6Knockout Mice

PartⅠ Endogenous RBBP6was knocked down by RNA interference, and theprotein level of γH2AX was examinedObjective Exposure to cellular stresses to select appropriate cell models respondingto DNA damage. Endogenous RBBP6of the cell line was knocked down by RNAinterference, and the protein level of γH2AX was examined.Methods Appropriate cell models responding to DNA damage were successfullyselected through examining the protein level of γH2AX after cisplatin treated.Endogenous RBBP6of the cell line was knocked down by RNA interference,following the detecting γH2AX by Western Blot.Results After HeLa was treated with cisplatin, the endogenous protein level ofγH2AX was clearly increased. It was very similar that when endogenous RBBP6ofHeLa was knocked down, there was also markably increase of the γH2AX proteinlevel.Conclusions γH2AX was greatly increased after knocked down RBBP6, suggestingthat the decline of RBBP6results in DNA double-strand breaks.PartⅡ Examining the expression of γH2AX in RBBP6knockout mice embryoObjective Separate E7RBBP6knockout mice embryo, and examine the expression ofγH2AX. Methods Immunohistochemistry was utilized to examine the expression of γH2AX inE7RBBP6knockout mice embryo.Results γH2AX level was also notably upregulated in RBBP6-/-mice embryocompared with the wild-type littermates.Conclusions γH2AX was greatly increased after depletion of RBBP6, suggesting thatthe deficiency of RBBP6resulting DNA double-strand break and genome instability.These data also contribute to explain why RBBP6deficiency resulted in theembryonic lethality.