New paper: Mistranslation increases phenotypic variation

Our collaborative work (with Shashi Thutupalli’s lab at NCBS) on tracking mistranslation-induced phenotypic variability is now published! Protein sequences often differ because of underlying differences in DNA sequence (i.e. genetic mutations). However, making mistakes while building the protein can also introduce differences in the protein sequence, although at a low frequency. Proteins altered in this manner cannot be inherited, but do they affect fitness linked traits? Laasya, Parth and Godwin (from Shashi’s lab) carried out experiments with wild type and error-prone cells, to test whether non-heritable protein sequence diversity can affect variability in important aspects of bacterial fitness, such as cell division times and survival under stresses like starvation. We found that high protein sequence diversity (via high mistranslation) indeed increases phenotypic variability at the single cell level, and impacts phenotype and fitness at the population level. For more, read the excellent NCBS news article by rotation student Nivedita Mukherjee here, or read the paper! Image credit: Nivedita Mukherjee

New paper: Mistranslation can be good!

Our work on ‘useful’ mistakes in bacteria (E. coli) is finally out! Laasya and Parth found that making rebel proteins not encoded by our DNA can be a good thing. In cells that frequently make mistakes, the accumulated ‘junk’ proteins end up triggering a high alert situation. This allows the cells to better deal with various external assaults (like increased temperature, damage to DNA and so on). When everything is normal this isn’t a big deal; in fact the junk makes cells mildly sick.  Under stress though, the high alert and error prone cells get the upper hand, leaving behind the more accurate (but less prepared) regular cells. For more: read the paper, and an NCBS news article. And, enjoy this summary cartoon from Pranjal Gupta that was featured on the journal cover!