Noxa protein is a member of the Bcl2 protein family. Studies have shown that this protein plays an important role in p53-induced apoptosis, which induces apoptosis by causing mitochondrial dysfunction. However, no relevant studies have reported the function of this protein in early embryonic development.
Recently, the research team of Gui Jianfang, a scholar at the Institute of Hydrobiology, Chinese Academy of Sciences, revealed the dual function of Noxa protein in zebrafish embryo development. They first analyzed the expression pattern and found that the maternal NoxamNA and protein are present in the early embryo, and both are constantly expressed during embryonic development. Early studies have shown that zebrafish embryos develop into 75% of embryos (8 hours after fertilization) and undergo apoptosis. This indicates that Noxa protein has other functions in the early embryonic development of zebrafish. After specifically knocking down Noxa protein, it was found that the mitosis of zebrafish embryonic cells was inhibited.
"Further experiments show that Noxa protein regulates normal line division in zebrafish embryonic cells by inhibiting the expression of Wnt4b protein. After packaging was reduced by 75%, reducing the expression of Noxa protein inhibited the development of apoptosis. Subsequent studies have shown that Noxa protein first induces the expression of Bik protein, and then works with Bik protein to regulate zebrafish embryonic cell apoptosis. During this period, Noxa protein stops regulating cell line division. In the above two physiological processes, the two proteins Mcl1a and Mcl1b bind to the Noxa protein, thereby inhibiting the function of regulating cell division or apoptosis, so that the zebrafish embryo can develop stably and normally. These findings are the first to prove that Noxa protein is an important cell mitosis regulator in zebrafish embryonic development, and performs different functions at different stages of embryonic development.
The research was completed by doctoral student Zhong Jianxiang and others. The corresponding author is scholar Gui Jianfang. The research was funded by the National Basic Research "973" Program and the Knowledge Innovation Project of the Chinese Academy of Sciences.