Prof. Zhongdong Qiao
Project Description and Objectives
According to current studies, some paternally acquired traits induced by environmental factors can be retained in gametes and passed down to the offspring. The molecular mechanism underlying this phenomenon however remains unclear. Our previous studies showed that tobacco smoking/nicotine treatments can lead to abnormal sperm function, and these abnormalities have been associated with DNA methylation changes within some gene promoter regions. We also found that nicotine induced a depression-like phonotype in mice and elevated the DNA methylation level within the CpG island shore region of mmu-miR-15b in murine sperm. This epigenetic information is then passed down to the offspring and imprinted in the brain tissue leading to hyperactivity in the filial generation of mice. Based on prior studies, our project intends to firstly establish a mouse smoking and nicotine treatment model. Secondly, analyse the DNA methylation patterns and sncRNAs expressive profile in the spermatozoa of smoking and nicotine treatment mice and in the brain tissue of the offspring. Our project mainly involves the epigenetic information retained in murine mature spermatozoa after nicotine treatment, such as DNA methylation and sncRNAs. These may influence the embryonic development of the offspring. The molecular mechanism underlying this paternal transgenerational effect on the offspring mice will also be illustrated, which can provide new evidence of the effects of paternal smoking on the physical and mental health of the offspring.
Interested students should have a basic knowledge of molecular biology.
Finish a program and write a research report
Give a research presentation: technical presentation.