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bioRxiv · 10.1101/2022.10.24.512971

A frameshift in Yersinia pestis rcsD leads to expression of a small HPt variant that alters canonical Rcs signalling to preserve flea-mammal plague transmission cycles

Guo, X.-P.·Yan, H.-Q.·Yang, W.·Yin, Z.·Vadyvaloo, V.·Zhou, D.·Sun, Y.-C.
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Abstract

Multiple genetic changes in the enteric pathogen Yersinia pseudotuberculosis have driven the emergence of Yesinia pestis, the arthropod-borne, etiological agent of plague. These include developing the capacity for biofilm-dependent blockage of the flea foregut to enable transmission by flea bite. Previously, we showed that pseudogenisation of rcsA, encoding a component of the Rcs signalling pathway, is an important evolutionary step facilitating Y. pestis flea-borne transmission. Additionally, rcsD, another important gene in the Rcs system, harbours a frameshift mutation. Here, we demonstrated that this rcsD mutation resulted in predominant production of a small protein composing the C-terminal RcsD histidine-phosphotransferase domain (designated RcsD-Hpt) and low levels of full-length RcsD. Genetic analysis revealed that the rcsD frameshift mutation followed the emergence of rcsA pseudogenisation. It further altered the canonical Rcs phosphorylation signal cascade, fine-tuning biofilm production to be conducive with retention of the pgm locus in modern lineages of Y. pestis. Taken together, our findings suggest that a frameshift mutation in rcsD, is an important evolutionary step that fine-tuned biofilm production to ensure perpetuation of flea-mammal plague transmission cycles.

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Guo, X.-P., Yan, H.-Q., Yang, W., Yin, Z., Vadyvaloo, V., Zhou, D., Sun, Y.-C.. 2022-10-25. A frameshift in Yersinia pestis rcsD leads to expression of a small HPt variant that alters canonical Rcs signalling to preserve flea-mammal plague transmission cycles. https://doi.org/10.1101/2022.10.24.512971

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