Dataset Information

Resistance Strategies Differ Against Specialist and Generalist Cyanophages

ABSTRACT: Long-term coexistence between cyanobacteria and their lytic viruses (cyanophages) in the oceans is thought to be due to the presence of sensitive cells in which cyanophages reproduce, ultimately killing the cell, while other cyanobacteria survive due to resistance to infection. Here we investigated resistance strategies in naturally resistant cyanobacteria and compared strategies against generalist and specialist cyanophages. Resistance was extracellular in most interactions against specialist cyanophages, preventing entry into the cell. In contrast, resistance was intracellular in practically all interactions against generalist cyanophages. Intriguingly, the stage of intracellular arrest was interaction-specific, halting at various stages of the infection cycle. These findings unveil a heavy cost of promiscuous entry of generalist phages into non-host cells that is rarely paid by specialists, potential unknown mechanisms of intracellular resistance and that the range for viral-mediated horizontal gene transfer extends much beyond just hosts.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Escherichia Coli

TISSUE(S): Whole Body

SUBMITTER: Tamar Ziv

LAB HEAD: Debbie Lindell

PROVIDER: PXD013030 | Pride | 2019-08-12

REPOSITORIES: Pride

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Publications

Resistance in marine cyanobacteria differs against specialist and generalist cyanophages.

Zborowsky Sophia S Lindell Debbie D

Proceedings of the National Academy of Sciences of the United States of America 20190805 34

Long-term coexistence between unicellular cyanobacteria and their lytic viruses (cyanophages) in the oceans is thought to be due to the presence of sensitive cells in which cyanophages reproduce, ultimately killing the cell, while other cyanobacteria survive due to resistance to infection. Here, we investigated resistance in marine cyanobacteria from the genera <i>Synechococcus</i> and <i>Prochlorococcus</i> and compared modes of resistance against specialist and generalist cyanophages belonging ...[more]

PMID: 31383764

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Project description:Here we exploit the essential process of X-chromosome dosage compensation to elucidate basic mechanisms that control the assembly, genome-wide binding, and function of gene regulatory complexes that act over large chromosomal territories. We demonstrate that a subunit of C. elegans MLL/COMPASS, a gene-activation complex, acts within the dosage compensation complex (DCC), a condensin complex, to target the DCC to both X chromosomes of hermaphrodites and thereby reduce chromosome-wide gene expression. The DCC binds to two categories of sites on X: rex sites that recruit the DCC in an autonomous, sequence- dependent manner, and dox sites that reside primarily in promoters of expressed genes and bind the DCC robustly only when attached to X. We find that DCC mutants that abolish rex-site binding do not eliminate dox-site binding, but instead reduce it to the level observed at autosomal binding sites in wild-type animals. Changes in DCC binding to these non-rex sites occur throughout development and correlate with transcriptional activity of adjacent genes. Moreover, autosomal DCC binding is enhanced by rex-site binding in cis in X-autosome fusion chromosomes. Thus, dox and autosomal sites exhibit similar binding properties. Our data support a model for DCC binding in which low-level DCC binding at dox and autosomal sites is dictated by intrinsic properties correlated with high transcriptional activity. Sex-specific DCC recruitment to rex sites then greatly elevates DCC binding to dox sites in cis, which lack intrinsically high DCC affinity on their own. We also show here that the C. elegans DCC achieves dosage compensation through its effects on transcription. ChIP-chip experiments using antibodies against DPY-27, SDC-3, DPY-30, DPY-26, MIX-1, SMC-4, ASH-2 in wild-type embryos. ChIP-chip experiments using antibodies against SDC-3, DPY-27, DPY-30, ASH-2, and IgG in different DCC mutants. ChIP-chip experiments using antibodies against RNA Pol II (hypophosphorylated and S2 and S5) in wild type and sdc-2 partial loss of function mutants.

Dataset Information

Resistance Strategies Differ Against Specialist and Generalist Cyanophages

Publications

Resistance in marine cyanobacteria differs against specialist and generalist cyanophages.

Similar Datasets

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