Prof. Zhongdong Qiao
Asso.Prof. Wangjie Xu
Project Description and Objectives
According to the present studies, some paternal acquired traits induced by environmental factors can be retained in gametes and passed down to the offspring. The underlying molecular mechanism underlying this phenomenon remains unclear. Our previous studies showed that tobacco smoking / nicotine treatment can lead to abnormal sperm function, and these abnormalities are associated with the 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 then passed down to the offspring and imprinted in the brain tissue leading to hyperactivity in the filial generation mice.
The objective of the project is to firstly establish a mouse smoking and nicotine treatment model and then analyze the DNA methylation patterns and sncRNAs expressive profile in the spermatozoa of smoking and nicotine treated mice and in the brain tissue of the offspring. Our project is mainly involved in the epigenetic information retained in murine mature spermatozoa after nicotine treatment, such as DNA methylation and sncRNAs which may influence the embryonic development of the offspring. The molecular mechanism underlying this paternal transgenerational effects on the offspring mice will also be illustrated which can provide new valid evidence of the effects of paternal smoking on the physical and mental health of the offspring
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