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Transcriptomic response during phage infection of a marine cyanobacterium under phosphorus‐limited conditions

Xingqin Lin; Huiming Ding; Qinglu Zeng
Environmental Microbiology · Vol. 18, Issue 2 · pp. 450-460 · 2016

Abstract

Summary The transcriptomic responses of bacteria to environmental stresses have been studied extensively, yet we know little about how the stressed cells respond to bacteriophage infection. Here, we conducted the first whole transcriptome sequencing (RNA‐seq) study of stressed bacteria to phage infection by infecting the marine picocyanobacterium P rochlorococcus NATL2A with cyanomyovirus P ‐ SSM 2 under P limitation, a strong selective force in the oceans. Transcripts of the P ‐acquisition genes in the uninfected cells were enriched after P limitation, including the high‐affinity phosphate‐binding protein gene pstS . They were still enriched in the infected cells under P ‐limited conditions. In contrast, transcripts of adenosine triphosphate (ATP) synthase and ribosomal protein genes were depleted in the uninfected cells after P limitation but were enriched during phage infection of P ‐starved cells. Cyanophage P ‐SSM2 contains pstS , and pstS and its adjacent gene g247 of unknown function were the only phage genes that were enriched under P ‐limited conditions. We further found that the host pstS transcript number per cell decreased after infection, however, it was still much higher in the P ‐limited infected cells than that in the nutrient‐replete cells. Moreover, phage pstS transcript number per cell was ∼20 times higher than the host copy, which may help maintain the host phosphate uptake rate during infection.

Bibliographic Information

JournalEnvironmental Microbiology
PublisherWiley
Publication Date2016-02-01
Publication Year2016
Volume18
Issue2
Pages450-460
Document TypeJournal Article
Print ISSN1462-2912
eISSN1462-2920
DOI10.1111/1462-2920.13104
SubjectMicrobial Ecology

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NARA Access Coverage1999-01-01~Current
Journal Homepagehttps://onlinelibrary.wiley.com/loi/14622920
Publisher PageOpen Publisher Page
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