<p>Abstract</p> <p>Background</p> <p>Abortive infection (Abi) mechanisms comprise numerous strategies developed by bacteria to avoid being killed by bacteriophage (phage). <it>Escherichia coli </it>Abis are considered as mediators of programmed cell death, which is induced by infecting phage. Abis were also proposed to be stress response elements, but no environmental activation signals have yet been identified. Abis are widespread in <it>Lactococcus lactis</it>, but regulation of their expression remains an open question. We previously showed that development of AbiD1 abortive infection against phage bIL66 depends on <it>orf1</it>, which is expressed in mid-infection. However, molecular basis for this activation remains unclear.</p> <p>Results</p> <p>In non-infected AbiD1+ cells, specific <it>abiD1 </it>mRNA is unstable and present in low amounts. It does not increase during abortive infection of sensitive phage. Protein synthesis directed by the <it>abiD1 </it>translation initiation region is also inefficient. The presence of the phage <it>orf1 </it>gene, but not its mutant AbiD1<sup>R </sup>allele, strongly increases <it>abiD1 </it>translation efficiency. Interestingly, cell growth at low temperature also activates translation of <it>abiD1 </it>mRNA and consequently the AbiD1 phenotype, and occurs independently of phage infection. There is no synergism between the two <it>abiD1 </it>inducers. Purified Orf1 protein binds mRNAs containing a secondary structure motif, identified within the translation initiation regions of <it>abiD1</it>, the mid-infection phage bIL66 M-operon, and the <it>L. lactis osmC </it>gene.</p> <p>Conclusion</p> <p>Expression of the <it>abiD1 </it>gene and consequently AbiD1 phenotype is specifically translationally activated by the phage Orf1 protein. The loss of ability to activate translation of <it>abiD1 </it>mRNA determines the molecular basis for phage resistance to AbiD1. We show for the first time that temperature downshift also activates abortive infection by activation of <it>abiD1 </it>mRNA translation.</p
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