Imprinting Analysis Of Qpct And Expression Profile And Study Of The Regulationthe Mechanism In Mouse

Qpct is a potential tumor suppressor gene, it can code the precursor of glutamic acylcyclization enzyme (QC). QC is a Zn++dependent acyl transferase, it has a alpha helix/β folded piece of structure. Qpct which code glutamic acyl cyclase can catalytic the N-teminal of glutamic acy to be pyroglutamic acid (pE). Once pE is gathered quickly, the role of the poison to the nervous system has been actived. Recent research demonstrated that amyloid is the reason of AD disease(Alzheimer disease).Through the report of NCBI, Qpct is located in the17chromosome of the mouse. It has seven exons, and the genomic location is chr:79451246-79489583. In order to clarify the difference expression of Qpct during the mouse embryonic development stage, the imprinting state is confirmed in the embryo and extraembryonic tissues with SNP-based PCR products sequencing analysis. At the same time, in situ hybridization and RT-PCR were used to detect the gene expression patterns. By sequencing, Qpct was identified as an imprinted gene in E15.5mouse. Moreover it is a placenta specific maternal expression imprinted gene. From E9.5-E11.5, Qpct was expressed abundantly in brain. At E10.5, the stronger signal is detected in otocyst. It also be detected in heart. At E15.5, Qpct is expressed in brain, tongue, liver, lung, intestinal and dorsal root ganglia, which the highest expression is brain and pituitary, followed by liver and dorsal root ganglion. In the placenta, during E12.5and E14.5development stage, the gene expression gradually increased and then decreased. In situ hybridization data show that Qpct is mainly expressed in spongioblast and labyrinthine at E12.5’s placenta, but Qpct is mainly expressed in decidua. What’s more, the imprinting mechanism is preliminary studied. Finally, it is confirmed that the CpG island is not the regulation mechanism. By the technology of ChIP, H3K9me3has not been the regulation mechanism of imprinting.