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<metadata xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:dc="http://purl.org/dc/elements/1.1/"><dc:title>A small bacteriophage protein determines the hierarchy over co-residential jumbo phage in Bacillus thuringiensis serovar israelensis</dc:title><dc:creator>Pavlin,	Anja	(Avtor)
	</dc:creator><dc:creator>Lovše,	Anže	(Avtor)
	</dc:creator><dc:creator>Bajc,	Gregor	(Avtor)
	</dc:creator><dc:creator>Otoničar,	Jan	(Avtor)
	</dc:creator><dc:creator>Kujović,	Amela	(Avtor)
	</dc:creator><dc:creator>Lengar,	Živa	(Avtor)
	</dc:creator><dc:creator>Gutiérrez-Aguirre,	Ion	(Avtor)
	</dc:creator><dc:creator>Kostanjšek,	Rok	(Avtor)
	</dc:creator><dc:creator>Konc,	Janez	(Avtor)
	</dc:creator><dc:creator>Fornelos,	Nadine	(Avtor)
	</dc:creator><dc:creator>Butala,	Matej	(Avtor)
	</dc:creator><dc:subject>bacteriophages</dc:subject><dc:subject>DNA damage</dc:subject><dc:subject>DNA repair</dc:subject><dc:description>Bacillus thuringiensis serovar israelensis is the most widely used biopesticide against insects, including vectors of animal and human diseases. Among several extrachromosomal elements, this endospore-forming entomopathogen harbors two bacteriophages: a linear DNA replicon named GIL01 that does not integrate into the chromosome during lysogeny and a circular-jumbo prophage known as pBtic235. Here, we show that GIL01 hinders the induction of cohabiting prophage pBtic235. The GIL01-encoded small protein, gp7, which interacts with the host LexA repressor, is a global transcription regulator and represses the induction of pBtic235 after DNA damage to presumably allow GIL01 to multiply first. In a complex with host LexA in stressed cells, gp7 down-regulates the expression of more than 250 host and pBtic235 genes, many of which are involved in the cellular functions of genome maintenance, cell-wall transport, and membrane and protein stability. We show that gp7 homologs that are found exclusively in bacteriophages act in a similar fashion to enhance LexA’s binding to DNA, while likely also affecting host gene expression. Our results provide evidence that GIL01 influences both its host and its co-resident bacteriophage.</dc:description><dc:date>2022</dc:date><dc:date>2024-01-19 12:36:44</dc:date><dc:type>Članek v reviji</dc:type><dc:identifier>154019</dc:identifier><dc:identifier>UDK: 579.6</dc:identifier><dc:identifier>ISSN pri članku: 2399-3642</dc:identifier><dc:identifier>DOI: 10.1038/s42003-022-04238-3</dc:identifier><dc:identifier>COBISS_ID: 132540419</dc:identifier><dc:language>sl</dc:language></metadata>
