# Characterization of MreCD in Streptococcus mutans

## TL;DR

This study explores the role of MreCD proteins in shaping and functioning of Streptococcus mutans, a bacteria linked to tooth decay.

## Contribution

The study identifies MreCD as key players in cell elongation and biofilm formation in S. mutans.

## Key findings

- Cells lacking mreCD were rounder, indicating a role in cell elongation.
- MreCD interacts with proteins involved in cell elongation and alters surface proteomes.
- Loss of mreCD affects biofilm architecture and bacteriocin gene expression.

## Abstract

Activities that control cell shape and division are critical for the survival of bacteria. However, little is known about the circuitry controlling these processes in the dental caries pathogen Streptococcus mutans.

We designed experiments to characterize two genes, mreC and mreD, in S. mutans. Assays included cell morphology imaging, protein interaction analysis, transcriptomics, proteomics, and biofilm studies to generate a comprehensive understanding of the role of MreCD in S. mutans

Consistent with mreCD participating in cell elongation, cells lacking these genes were found to be rounder than wild-type cells. Using bacterial two-hybrid assays, interactions between MreCD and several other proteins implicated in cell elongation were observed. Further characterization, using proteomics, revealed that the surface-associated proteome is different in mutants lacking mreCD. Consistent with these changes we observed altered sucrose-mediated biofilm architecture. Loss of mreCD also had a noticeable impact on bacteriocin gene expression, which could account in part for the observation that mreCD mutants had a diminished capacity to compete with commensal streptococci.

Our results provide evidence that cell elongation proteins are required for normal S. mutans physiology and establish a foundation for additional examination of these and related proteins in this organism.