Nanda Kumar Jegadesan - ESR 3
Name: Nanda Kumar Jegadesan
Nationality: Indian
Main Host Institution: IFOM Foundation - The FIRC Institute of Molecular Oncology Foundation
Academic Background: In 2015, I have completed my Master’s degree in Genomics from the School of Biological Sciences, Madurai Kamaraj University, Madurai, India
After completion of my Master’s I have joined as research fellow, enrolled in a project to decipher the function Long Non-coding RNAs in cancer in CSIR-Institute of Genomics and Integrative Biology, New Delhi, India.
Project title: Molecular analysis of the replication stress response caused by DDX11 dysfunction and overexpression
Project background: Faithful chromosomal DNA replication is critical for normal development and genome stability. An important and prevalent source of genome instability in cancers is replication stress. Multiple activities cooperate to mitigate replication stress, either by regulating DNA dynamics at sites of replication stress or by coordinating DNA replication with the establishment of chromatin and chromosome structure. Recently our lab, characterized the roles of DDX11— an evolutionarily conserved iron-sulfur cluster helicase that is mutated in the Warsaw breakage syndrome (WABS) —, in sister chromatid cohesion and in replication-associated repair. It is essential for embryonic development in mouse and for survival of melanoma cells, suggesting critical roles of DDX11 in proliferation and tumorigenesis. Moreover, DDX11 is mutated and overexpressed in multiple cancers, including breast and ovarian cancers, and its expression influences DNA damage tolerance towards drugs often used in chemotherapy.
Project Aim: The goal of our project is to understand and decipher the underlying molecular mechanism of DDX11 in maintenance of telomere and genome integrity by applying various techniques like CRISPR/CAS9 mediated genome editing technology, telomere fish and electron microscopy etc., we also plan to perform screening to identify genes required for viability under normal conditions or in the presence of DNA damaging drugs from the DDX11 upregulation and downregulation background cancer cell lines.
Expected outcome: The results of these studies will advance our understanding of cell division, chromatin structure and cohesion regulation at the nexus with DNA replication. The findings will also provide insight into genes that function in the same pro-proliferative/pro-survival pathway as DDX11, and indicate new potential targets for cancer therapy
Contact: https://www.ifom.eu/en/cancer-research/research-labs/research-lab-branzei.php