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Scientists brand singular cell-signaling complement in some S. pneumoniae strains

 

A scanning nucleus micrograph of Streptococcus pneumoniae (Pneumococcus; Streptococci). Credit: phil.cdc.gov; Janice Haney Carr

Some strains of Streptococcus pneumoniae—a disease-causing bacterium—possess a cell-to-cell signaling complement that might change gene countenance and distress in co-colonizing strains, according to a investigate published in PLOS Pathogens.

S. pneumoniae is widespread in a tellurian respiratory tract, though customarily does not means any symptoms. However, in children and a elderly, it is a vital means of pneumonia, meningitis, and other potentially lethal diseases. Of sold seductiveness is a organisation of S. pneumoniae strains famous as PMEN1, that are pestilence and multi-drug resistant.

To improved know what creates PMEN1 strains so successful, Anagha Kadam of Carnegie Mellon University, Pennsylvania, and colleagues achieved a genetic shade to brand genes hexed by PMEN1 strains, though not by other strains. This suggested that roughly all PMEN1 strains have a singular genomic segment consisting of several specific genes.

The group found that dual of these genes, phrA2 and tprA2, correlate to umpire S. pneumoniae gene expression. The protein encoded by tprA2 inhibits countenance of phrA2 and other adjacent genes, including a gene famous as lcpA. In mice, a researchers found, a TprA2 protein does not impact S. pneumoniae colonization in a nasopharynx, though it does strengthen opposite lung infection. The commentary advise that this is a outcome of TprA2’s control over lcpA expression.

Meanwhile, a phrA2 protein product relieves a inhibitory effects of TprA2, augmenting lcpA expression. phrA2 countenance is aloft when a firmness of cells in an S. pneumoniae cluster is higher. Evidence suggests that cells in high-density populations hide a phrA2 protein product, and this protein afterwards signals other cells to demonstrate phrA2.

Beyond a purpose in this novel TprA2/PhrA2 system, a PhrA2 protein also appears to be means to activate a second, ancestral signaling complement that is widespread among S. pneumoniae, including in non-PMEN1 strains. This suggests that PMEN1 strains can change both their possess gene countenance and that of non-PMEN1 strains. This is rarely applicable given multi-strain infections are really common.

Phylogenetic research suggests that a genes in a TprA2/PhrA2 complement primarily found their approach into an ancestral PMEN1 aria by plane gene transfer, instead of being upheld from a dividing dungeon to a daughter cells. The authors note that this might be a initial instance of a horizontally eliminated regulatory complement that has integrated with ancestral network to concede gene law opposite strains.


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More information:
Kadam A, Eutsey RA, Rosch J, Miao X, Longwell M, Xu W, et al. (2017) Promiscuous signaling by a regulatory complement singular to a pestilence PMEN1 pneumococcal lineage. PLoS Pathog 13(5): e1006339. DOI: 10.1371/journal.ppat.1006339

Journal reference:
PLoS Pathogens

Provided by:
Public Library of Science

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