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RNA-seq of Pectobacterium carotovorum subsp. carotovorum and P. polaris infecting potato at 24, 48 and 72 hpi, and grown on M9 solid minimal medium at 24 hpi

ABSTRACT: RNA-seq of Pectobacterium carotovorum subsp. carotovorum and P. polaris infecting potato at 24, 48 and 72 hpi, and grown on M9 solid minimal medium at 24 hpi

PROVIDER: PRJEB32362 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR3300850_1.fastq.gz	Fastqsanger.gz
	ERR3300850_2.fastq.gz	Fastqsanger.gz
	ERR3300860_1.fastq.gz	Fastqsanger.gz
	ERR3300860_2.fastq.gz	Fastqsanger.gz
	ERR3300870_1.fastq.gz	Fastqsanger.gz

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RNA-seq of Pectobacterium carotovorum subsp. carotovorum and P. polaris infecting potato at 24, 48 and 72 hpi, and grown on M9 solid minimal medium at 24 hpi

Project description:Importance: Pectobacterium species cause soft rot in potato and other host plants primarily by secreting a battery of plant cell wall degrading enzymes. In addition, several different secretion systems are mobilized during infection. Previous studies of gene expression and regulation thereof primarily focused on the onset of infection. This work investigated transcriptome changes in Pectobacterium during the infection of potato tubers up to 72 hours post inoculation to elucidate biological processes during a longer infection period. Methods: The transcriptomes of aggressive strains of the two species P. carotovorum subsp. carotovorum and P. polaris were investigated during infection of potato minitubers (cv. 'Asterix') at 24, 48 and 72 hours after inoculation by RNA sequencing. The transcriptomes were compared to that of bacteria grown on minimal M9 medium, and transcriptomes from later infection time points (48 and 72 hours after inoculation) were compared to early infection (24 hours after inoculation). Results: Plant cell wall degrading enzymes and secretion system associated genes were largely upregulated during infection compared to in vitro growth, but downregulated in the later phases of infection compared to the early infection phase. The downregulation was not sufficiently explained by the expression of known virulence regulators such as the RsmA/B or the ExpA/S systems.

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