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Bendori, S. O.

Publications and source records attributed to Bendori, S. O..

3 recordsLinked to original sources

A phage communication peptide alters Bacillus subtilis colony development and promotes sporulation

Temperate Bacillus phages use arbitrium peptides to coordinate lysis-lysogeny decisions, but whether the mature communication peptide can be sensed directly by Bacillus subtilis and affect its physiology and behavior is unknown. Here we show that the {varphi}3T arbitrium peptide SAIRGA elicits a sequence- and stereochemistry-dependent response in Bacillus subtilis that is strongly expressed in surface-grown colony biofilms but is not accompanied by comparable changes in planktonic growth or static-liquid pellicle morphology. The response persists in the absence of AimR, the canonical arbitrium receptor. Within colonies, SAIRGA alters spatial PtapA activity and increases heat-resistant spore formation without increasing total viable cell yield. Untargeted metabolomics reveals broad dose-dependent remodeling that tracks peptide activity, while program-level proteomics independently converges on late-sporulation and mature-spore-associated states. This study highlights how a phage-derived peptide may act as a signal, enabling the host to pivot toward a survival-focused developmental state.

microbiology↗

An unprecedented DNA recognition-mimicry switch governs induction in arbitrium phages

Temperate phages integrate multiple information sources to regulate lysis-lysogeny transitions. SPBeta-like phages use arbitrium signalling and DNA damage to control repressor activity during lytic induction, but how the repressor functions and is inactivated by the SOS response remains unclear. Here, we show that SroF, the SPBeta-like phage repressor, binds DNA via a novel mechanism involving its integrase-like fold, enabling stable prophage repression. Upon DNA damage, the host SOS response triggers derepression of a newly identified antirepressor, Sar. Sar binds SroF by mimicking the DNA structure recognised by the repressor, inactivating its function and inducing phage. This mechanism is conserved across SP{beta}-like phages, which encode multiple, specific SroF-Sar pairs. Surprisingly, repressor inactivation alone is insufficient for induction when arbitrium levels are high. Our results uncover the mechanism underlying the double layer of control that ensures phage induction occurs only under SOS conditions and in the absence of neighbouring prophages.

molecular biology↗

Arbitrium systems control lysis/lysogeny through the regulation of small antirepressor proteins

Many temperate Bacillus phages utilize the arbitrium signaling system to control lysis/lysogeny decisions. While the function of the arbitrium signal AimP and its receptor AimR are well known, it is unclear how they control lysis in most arbitrium systems. Here, we show that a large majority of arbitrium systems are embedded in an extended module with three additional components; A small antirepressor protein (AimX), the phage repressor (AimC) and an adjacent cro-like protein (AimL). AimR-dependent activation of AimX is necessary for lysis both during infection and lytic induction. Molecular analysis suggests that AimX directly binds AimC and prevents its oligomerization and binding to its regulated aimL promoter. Our work therefore uncovers the main mechanism by which arbitrium systems regulate lysis and point to the central role of small proteins in phage decision making. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=176 SRC="FIGDIR/small/689978v1_ufig1.gif" ALT="Figure 1"> View larger version (35K): org.highwire.dtl.DTLVardef@63dd49org.highwire.dtl.DTLVardef@54e7ecorg.highwire.dtl.DTLVardef@466235org.highwire.dtl.DTLVardef@d98ef2_HPS_FORMAT_FIGEXP M_FIG C_FIG

microbiology↗