Blog

For more Information about Professor Kundan Sengupta and his Team click the picture above.

Read the following Abstract from Prof. Sengupta to get more Informations about his upcoming Talk:

Role of nuclear lamins in regulating chromosomal instability in cancer cells
Kundan Sengupta
Chromosome Biology Lab (CBL), Indian Institute of Science Education and Research (IISER),
Pune, INDIA
Lamins are type V intermediate filament proteins crucial for maintaining the structure and
func7on of the nucleus. When lamins are depleted, nuclear morphology is significantly
altered. Furthermore, loss of lamins also causes chromosomal gains. These aneuploid
chromosome territories show altered localization in the interphase nucleus, indicating that
lamins not only maintain nuclear morphology but also stable chromosomal organization and
function. This is consistent with increased chromatin dynamics in cells where lamins are
depleted. Interestingly, overexpression of the transcription factor Twist1, which usually
induces Epithelial-Mesenchymal Transitions (EMT), decreases lamin levels accompanied by
an increase in nuclear blebs, micronuclei, and DNA damage in colorectal cancer cells. On the
other hand, depletion of the Lamin B receptor (LBR), a direct interactor of B-type lamins,
reveals a specific pattern of chromosomal losses that are consistently enriched within the
micronucleus. In marked contrast, the depletion of the Lamin B receptor (LBR) – a direct
interactor of B-type lamins, uncovered a specific pattern of chromosomal losses that were
not only mislocalized in the 3D interphase nucleus but were enriched within nuclear blebs
and micronuclei. We uncovered a novel mechanism involving LBR and the Telomere
Recognition Factor (TRF) in the maintenance of diploid chromosome numbers in colorectal
cancer cells. In conclusion, lamins play an essential role in protecting nuclear organization,
chromosomal stability, and genome function, involving novel partners of the lamin
interactome.