Name：Jia-Min Zhang

Title：Professor

E-mail:zhangjiamin@tongji.edu.cn

Tel: (+86)-021 65981567

Address: School of Life Sciences and Technology, Tongji University, 1239 Siping Road, Yangpu District, Shanghai 200092, China

Google Scholar: https://scholar.google.com/citations?user=rlXB-cwAAAAJ&hl=en

Areas of interest: Genome stability, Epigenetics, Gene regulatory networks

General Info

Research Experience

2022 – Present    Professor, School of Life Sciences and Technology, Tongji University, Shanghai, China

2021-Present       Principal Investigator, Tongji Hospital, Shanghai, China

2021– 2022         Principal Investigator, School of Life Sciences and Technology, Tongji University, Shanghai, China

2015 – 2020        Postdoctoral Research Fellow, Massachusetts General Hospital Cancer Center, Harvard medical school, Boston, MA, USA

2013 - 2015         Postdoctoral Research Fellow, National Institute of Biological Sciences (NIBS), Beijing, China

Education

2013                    Ph.D. Biochemistry and Molecular Biology, National Institute of Biological Sciences (NIBS), Beijing, China

2008                    B.S.A., China Agricultural University, China

Research Interests

· Molecular Mechanisms of Telomere Maintenance and DNA Damage Repair:

Investigate the intricate processes that govern telomere maintenance and DNA damage repair, essential for preserving genome integrity. This includes exploring the mechanism of alternative lengthening of telomeres (ALT) pathway in cancer cells, and the mechanisms by which cells detect and repair DNA damage at telomeres. The goal is to elucidate how defects in these processes contribute to cancer and aging, and to identify potential therapeutic targets for intervention.

· Development of New Technologies for Chromatin Epigenetic Detection:

Innovating and refining cutting-edge technologies to detect and analyze chromatin landscape. These tools aim to provide deeper insights into the regulatory mechanisms at play in normal development and disease, particularly in cancer, and to enable high-resolution, single-cell, and multi-omics analyses.

· Gene Regulatory Networks (GRNs) in Development and Disease: 

Constructing and analyzing gene regulatory networks to understand how genes are regulated during development and how dysregulation contributes to disease. This research leverages deep learning and multi-omics data to map the complex Gene Regulatory Networks that drive both normal and pathological processes.

Representative Publications

1. Ouyang, J., Yadav, T., Zhang, J.M., et al. (2021). RNA transcripts stimulate homologous recombination by forming DR-loops. Nature, 594, 283-288.

· This study proposed a new mechanism where RNA transcripts participate in activating homologous recombination repair.

2. Zhang, J.M., Genois, M.M., Ouyang, J., et al. (2021). Alternative lengthening of telomeres is a self-perpetuating process in ALT-associated PML bodies. Molecular Cell, 81, 1–16.

· The study built an inducible APB system to study ALT pathways and proposed a new model of self-reinforcing signaling loops in the ALT pathway.

3. Zhang, J.M., Yadav, T., Ouyang, J., et al. (2019). Alternative Lengthening of Telomeres through Two Distinct Break-Induced Replication Pathways. Cell Reports, 26, 955-968 e953.

· This study developed a new method for real-time tracking of ALT telomere DNA synthesis and proposed a dual-pathway model of ALT homologous recombination.

4. Chen, H., Chen, H., Zhang, J.M., et al. (2020) cGAS suppresses genomic instability as a decelerator of replication forks. Science Advances, 14 Oct 2020: Eabb8941.

· This study discovered that cGAS plays an important role in responding to DNA replication stress, independent of the STING pathway.

5. Shin, S.H., Lee, J.S., Zhang, J.M., et al. (2020). Synthetic lethality by targeting the RUVBL1/2-TTT complex in mTORC1-hyperactive cancer cells. Science Advances, 6, eaay9131.

· This study revealed that RUVBL1/2 may be a therapeutic target for cancers with high mTORC1 levels, offering new strategies for cancer-targeted therapy.

6. Zhang, J.M., Zheng, J.X., Ding, Y.H., et al. (2020). CRL4Cdt2 ubiquitin ligase regulates Dna2 and Rad16 (XPF) nucleases by targeting Pxd1 for degradation. PLOS Genetics, 16, e1008933.

· The study discovered new functions of CRL4 E3 ligase in DNA damage repair and linked ubiquitination systems with nucleases' spatiotemporal regulation.

7. Zhang, J.M., and Zou, L. (2020). Alternative lengthening of telomeres: from molecular mechanisms to therapeutic outlooks. Cell & Bioscience, 10, 30.

· This review summarizes recent advances and future perspectives in the ALT research field.

8. Matos, D.A., Zhang, J.M., Ouyang, J., et al. (2020) ATR protects the genome against R loops through a MUS81-triggered feedback loop. Molecular Cell, 77, 514-527 e514.

· This study elucidated the role of ATR in maintaining DNA replication fork stability in response to R-loops.

9. Zhang, J.M., Liu, X.M., Ding, Y.H., et al. (2014). Fission yeast Pxd1 promotes proper DNA repair by activating Rad16XPF and inhibiting Dna2. PLOS Biology, 12, e1001946.

· The study revealed a new mechanism of coordinated regulation between nucleases, highlighting the balance between DNA repair capability and genome stability.

The lab is actively recruiting postdoctoral researchers and graduate students. Interested Ph.D. and Master's candidates, as well as undergraduates, are welcome to apply for positions and internships.