My name is Shivani Ramakrishnan, and I am from India. I graduated with a dual degree (BS-MS) in Biology from the Indian Institute of Science Education and Research (IISER) Thiruvananthapuram, India. For my master’s thesis, I studied how centriole number is regulated during the G1/S phase by controlling the levels of a protein called STIL.

I then worked as a research assistant at Institut Curie, France, where I focused on in vitro studies exploring the interaction between human tau protein, microtubules, and kinesin motors, and how these interactions may contribute to neurodegeneration.

As a Ph.D student in Lotte’s lab, I will investigate the roles of two proteins, CCDC92 and CCDC198, in ciliary protein trafficking and extracellular vesicle (EV) biology. My project will focus on understanding how these proteins localize and traffic within cells and cilia, identifying their key interaction partners, and exploring how mutations impact ciliary protein composition, EV release, and signaling.

In my free time, I enjoy watching movies and series, singing, cooking Indian food, spending time with friends, and exploring the city.

Dissecting the functional interactions between primary cilia, extracellular vesicles, and endo-lysosomal pathways

The group has recently identified that CCDC198 and CCDC92 localize to primary cilia and extracellular vesicles (EVs) of kidney epithelial cells, hinting at possible roles in ciliary trafficking/signalling. Thus, the broad aim of the project is to look at the ciliary functions and dynamics of these two proteins. Using cultured mammalian (kidney) cell models and advanced molecular imaging and biochemical techniques, we aim to answer the following questions: 1) How does the loss of CCDC198 and CCDC92 affect ciliary and cellular ultrastructure; 2) How do these proteins localize and traffic within cells and cilia, and what are their key interaction partners; 3) How do mutations in these proteins affect ciliary protein composition, EV release and signalling? The results of this project will provide new insight into the mechanisms underlying EV release by primary cilia, and how perturbation of these mechanisms may contribute to disease pathology of ciliopathies.