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Seminars and Colloquia


Hijacking physiological pathways for pathological outcomes 
Mon, Mar 12, 2018,   12:00 PM to 01:00 PM at Seminar Room 34, 2nd Floor, Main Building

Dr. Pavithra L Chavali
MRC Laboratory of Molecular Biology, UK

A fine balance between cell death and division maintains cellular homeostasis and facilitates organismal survival and growth. Increase in cell death or reduction in cell division results in hypocellularity and manifests as global growth defects such as primordial dwarfism or developmental defects of specific organs. On the contrary, an increase in cell division and/or reduction in cell death might result in hypercellularity, as seen in cancers. During normal development, the cell cycle machinery has two important tasks–to ensure (i) maintenance of genome integrity and (ii) that cell division occurs in a temporally controlled fashion. This is best exemplified in the developing fetal brain, wherein defective cell division or cell death can lead to impaired brain size and function. Autosomal primary recessive microcephaly (MCPH) is one such neurodevelopmental disorder resulting in reduced brain size at birth. MCPH has been attributed to the loss of functions of atleast 12 different genes, all of which at some point of cell cycle remain associated with the cell division machinery, namely centrosomes. In my talk, I will discuss about my recent findings providing mechanistic insights into the regulation of cell division by two different MCPH genes and how mutations in them lead to microcephaly. Finally, I will discuss how these mechanisms essential for normal brain development are hijacked by cancers or by viruses for their survival [1, 2].  


  1. Chavali PL et al., A CEP215-HSET complex links centrosomes with spindle poles and drives centrosome clustering in cancer. Nature Communications 2016; 7: 11005.
  2. Chavali PL et al., Neurodevelopmental protein Musashi1 interacts with the Zika genome and promotes viral replication. Science 2017; 375: 83-88.