Faculty

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Yan ZHAO
Associate Professor
0755-88015840
zhaoyan@sustech.edu.cn

Introduction

Dr. Zhao received her bachelor’s and Ph.D. degree from Peking University Health Science Center, followed by postdoctoral research at the Institute of Biophysics, Chinese Academy of Sciences and UMass Medical School. She joined SUSTech as an assistant professor in 2020. Dr. Zhao mainly focuses on studying the molecular mechanism and physiological function of metazoan-specific autophagy genes. Previous research outputs have been published in high-impact international journals, including Molecular Cell, Current Biology, JCB, Autophagy, Cell reports etc.

 

Research Interests

Autophagy is an evolutionarily conserved cell surveillance system that removes toxic protein aggregates and damaged organelles to maintain cellular homeostasis, especially in postmitotic cells like neurons. Dysregulation of autophagy has been linked with various human diseases, such as neurodegenerative diseases, cancer and diabetes. Our team has particular interest in understanding the molecular role and in vivo function of metazoan-specific autophagy proteins, by integrating techniques in cell biology, biochemistry, CRISPR gene editing and mouse genetics. Our main research areas include:

1. Studying how autophagy proteins collaborate with each other to regulate the ER contacts with preautophagosomal structures for autophagosome formation

2. Exploring the specific requirement of autophagy machinery to protect neural homeostasis and finding potential druggable targets for treating neurodegenerative diseases

3. Elucidating the molecular constituents, regulation and physiological function of ER contacts with other intracellular organelles

 

Selected Publication:

1. Ji, M., Li, M., Sun, L., Zhao, H., Li, Y., Zhou, L., Yang, Z., Zhao, X., Qu, W., Xue, H., Zheng, Z., Li, Y., Deng, H., and Zhao, Y.G. (2022) VMP1 and TMEM41B are essential for DMV formation during β-coronavirus infection. J Cell Biol 221, e202112081.

2. Ji, C., Zhao, H., Zhang, H., and Zhao, Y.G. (2021) β-propeller proteins WDR45 and WDR45B regulate autophagosome maturation into autolysosomes in neural cells. Curr Biol 31, 1666-1677.

3. Ji, C., Zhao, H., Li, D., Sun, H., Hao, J., Chen, R., Wang, X., Zhang, H., and Zhao, Y.G. (2020) Role of Wdr45b in maintaining neural autophagy and cognitive function. Autophagy 16, 615-625.

4. Li, D., Zhao, Y.G.*, Li, D., Zhao, H., Huang, J., Miao, G., Feng, D., Liu, P., Li, D., and Zhang, H. (2019) The ER-localized protein DFCP1 modulates ER-lipid droplet contact formation. Cell Rep27, 343-358. (*Zhao, Y.G. as co-first author)

5. Zhao, Y.G., Liu, N., Miao, G., Chen, Y., Zhao, H., and Zhang, H. (2018) The ER contact proteins VAPA/B interact with multiple autophagy proteins to modulate autophagosome biogenesis. Curr Biol28, 1234-1245.

6. Zhao, Y.G., Chen, Y., Miao, G., Zhao, H., Qu, W., Li, D., Wang, Z., Liu, N., Li, L., Chen, S., Liu, P., Feng, D., and Zhang, H. (2017) The ER-localized transmembrane protein EPG-3/VMP1 regulates SERCA activity to control ER-isolation membrane contacts for autophagosome formation. Mol Cell67, 974-989.

7. Zhao, Y.G., Sun, L., Miao, G.Y., Ji, C.C., Zhao, H.Y., Sun, H.Y., Miao, L., Yoshii, S.R., Mizushima, N., Wang X.Q., and Zhang, H. (2015) The autophagy gene Wdr45/Wipi4 regulates learning and memory function and axonal homeostasis. Autophagy11, 881-890.

8. Zhao, Y.G.*, Zhao, H.Y., Sun, H.Y., and Zhang, H. (2013) Role of Epg5 in selective neurodegeneration and Vici syndrome. Autophagy9, 1185-1189. (*Zhao, Y.G. as first author and co-corresponding author)

9. Zhao, H.Y., Zhao, Y.G.*, Wang, X.W., Xu, L.J., Miao, L., Feng, D., Chen, Q., Kovács, A.L. Fan, D.S., and Zhang, H. (2013) Mice deficient in Epg5 exhibit selective neuronal vulnerability to degeneration. J Cell Biol200, 731-741. (*Zhao, Y.G. as co-first author and co-corresponding author)

10. Zhao, Y.G., Zhao, H.Y., Miao, L., Wang, L., Sun, F., and Zhang, H. (2012) The p53-induced gene Ei24 is an essential component of the basal autophagy pathway. J Biol Chem 287, 42053-42063.