Bose Institute.Parul Chakrabarti - Basu's mentor at Bose Institute
Born on 17 December 1957[2] in the Indian state of West Bengal, Joyoti Basu did her undergraduate studies at the Presidency College, Kolkata and after completing the BSc honors in chemistry, she obtained an MSc from the University of Calcutta.[3] Her doctoral research was at the Bose Institute, Kolkata[4][5] under the guidance of Parul Chakrabarti, which earned her a PhD from Calcutta University. She did her post-doctoral work at the laboratory of Jean-Marie Ghuysen at the University of Liège working on mycobacterial cell division and mycobacterial peptidoglycan-biosynthesizing enzymes. She joined Bose Institute in 1991 as a faculty member at the department of Chemistry[6][7] and retired in June, 2018.
Basu resides along Madhab Chatterjee Street in Kolkata.[8]
Controversy
Basu's alleged scientific misconduct has been noted widely and has even been covered in media. She is widely alleged to have duplicated images leading to retraction of two papers, correction of another two, and, many alleged instances of misconduct listed on Pubpeer.[9] Basu has retracted a few of her papers.[10] This includes an article published in The Journal of Immunology.[11][12]
Legacy
Red Blood Cells
Basu's research is focused on the cellular and molecular biology of mycobacteria.[13] During the initial stages of her career, she worked on the membrane structure of red blood cells and her research is reported to have assisted in widening the understanding of apoptosis of nucleated mammalian cells and the physiology of the red cell that lacked a cell nucleus.[3] Her association with her mentor, Parul Chakrabarti, during her doctoral research days, precipitated the studies of the biosynthetic pathways of fatty acids in relation to cell wall building and the functions of penicillin-binding proteins.[14] She is known to be the first scientist to propose that the removal of the aged or oxidatively stressed red blood cells from the circulatory system causes cellular death. Later she moved on to the biological study of Mycobacterium tuberculosis, a pathogenic bacteria causing tuberculosis, with regard to its host-pathogen interaction and her studies revealed the mechanisms of macrophageapoptosis as well as the relationship between host cell signaling and innate immune response. In 2007, the team led by Basu and her college mate from the Presidency College, Manikuntala Kundu, were successful in identifying a protein in Mycobacterium tuberculosis which caused weakening of the immune system of the host.[15] They found that the protein, named Early Secreted Antigen 6, which bound themselves on Toll-like receptor 2 of the host, hindered the production of cytokines, a type of protein which helped the immune system to fight the tuberculosis bacteria. The discovery also has reported importance in the therapeutics of diseases like rheumatoid arthritis.[15] The achievement was later published as an article, Direct extracellular interaction between the early secreted antigen ESAT-6 of Mycobacterium tuberculosis and TLR2 inhibits TLR signaling in macrophages in Nature Immunology journal in 2007.[16] Her studies have been documented by way of a number of articles[17][note 1] and ResearchGate, an online repository of scientific articles has listed 77 of them.[18] Besides, she has mentored several research scholars in their doctoral studies.[19]
Basu is a member of the executive committee of the Indian Society of Cell Biology[20] and is a former Treasurer of the Society.[21][22] She is credited with contributing to the establishment of a program on Systems Biology at the Bose Institute. She is also a former associate editor of the Journal of Immunology and is an Academic Editor of PLoS One.[3]
^"NASI Year Book 2015"(PDF). National Academy of Sciences, India. 24 November 2017. Archived from the original(PDF) on 6 August 2015. Retrieved 24 November 2017.
^"INSA Year Book 2016"(PDF). Indian National Science Academy. 9 December 2017. Archived from the original(PDF) on 4 November 2016. Retrieved 9 December 2017.
