Ribosome stalling as gene regulation?

Another cool paper from Mankin lab showed up in Nature Chemical Biology. This time researchers were looking at the detailed mechanism of translational arrest by two macrolide antibiotics, erythromycin and telithromycin.


Via series of mutations authors identified a single amino acid in the nascent peptide chain that determines selectivity and promiscuity of ribosome stalling by either of two antibiotics. To prove their point, they created an unnatural mutant gene with engineered selectivity to TEL.

While major implications of the study are dealing with antibiotic resistance and ways to overcome it, the authors coin an interesting evolutionary speculation. They suggest that the ribosome stalling could be another mechanism for gene regulation. In this case the sequence of some peptides could evolve in order to recognize small molecules during translation of the protein itself. And this could be another way to react on the environmental stimuli.

I guess that calls for another whole-transcriptome and cross-species genomic mining study for identification of such sequence−cofactor pairs.

By the way, a rare case, they did molecular dynamics simulation but didn’t include any pretty picture from it in the main text of the manuscript! That’s what happening when one has enough experimental data.

Writing code for synthetic life

In the high school my chemistry teacher used to tell us that chemists do not only study the nature, but they also invent their own subject of study. The more I learn about biology, the more I feel that biologists move in the same direction, creating the new field of synthetic biology.

Recent report on the expansion of DNA alphabet by two letters grossly overshadowed not that press-release-friendly development in the synthetic biology of RNA. But there are quite some interesting things going on in the latter field that deserve as much attention. Continue reading “Writing code for synthetic life”