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Nijland, J. G.

Publications and source records attributed to Nijland, J. G..

2 recordsLinked to original sources

The infection cycle of the haloarchaeal virus HFTV1 is tightly regulated and strongly inhibits motility of its host

Although viruses have been shown to infect all domains of life, our understanding of the genetic program behind the exploitation of host resources to produce progeny virions is thus far limited to several bacterial viruses. Therefore, to elucidate the transcriptome of euryarchaeal viruses and their hosts, we employed RNAseq analysis of samples taken at different time points from Haloferax gibbonsii LR2-5 cultures infected with the lytic model virus Haloferax Tailed Virus 1 (HFTV1). While following the transcription of viral genes throughout the infective life cycle, we observed a tight temporal regulation of viral transcripts as well as differential expression from within viral gene clusters. Furthermore, anti-sense RNAs (asRNAs) appear to play an important role in support of the timing of late-expressed viral genes. Therefore, with many differentially expressed transcripts, including intragenic transcripts and asRNAs, the regulatory machinery employed by HFTV1 contrasts with viral model systems (based on phages), in which antitermination and/or alternative polymerases (seemingly lacking in HFTV1) are more widespread. When looking into differentially expressed host genes, we observed a strong downregulation of genes involved in motility, such as the archaellum and chemotaxis machinery, which was confirmed with swimming assays of HFTV1 infected cells. This might be a strategy of the virus to redirect energy flowing into movement towards the production of virions. In conclusion, this work thus provides a stepping stone for further exploration of the intriguing strategies of viral transcriptional regulation of their infection cycle across the domains of life. IMPORTANCEViruses infect members of all three domains of life, including Archaea. Euryarchaea are widespread microorganisms found in various environments such as the human gut and solar salterns. Due to the exceptional availability of cell biology and genetic tools of some salt-loving archaea, they are a model system to extrapolate from. Insights into the regulation of viral infections are of particular importance, especially since HFTV1, has been adopted as a model virus by the archaeal viral community. We found that, while harboring parallels with bacterial viruses, such as tight temporal regulation, HFTV1 harbors an impressive number of differentially expressed transcriptional units. Furthermore, anti-sense RNAs and intragenic regulatory elements seem to play a much more prominent role in HFTV1 gene expression. Thus, this work challenges current models and provides valuable new insights into the gene regulation of viral infection of archaea, which mark similarities and differences with viruses from other domains of life.

microbiology↗

The ethanol tolerance in Saccharomyces cerevisiae under a phenomics perspective

Ethanol (EtOH) is a substantial stressor for Saccharomyces cerevisiae. Data integration from strains with different phenotypes, including EtOH stress-responsive lncRNAs, are still not available. We covered these issues seeking systems modifications that drive the divergences between higher (HT) and lower (LT) EtOH tolerant strains under their highest stress conditions. We showed that these phenotypes are neither related to high viability nor faster population rebound after stress relief. LncRNAs work on many stress-responsive systems in a strain-specific manner promoting the EtOH tolerance. Cells use membraneless RNA/protein storage and degradation systems to endure the stress harming, and lncRNAs jointly promote EtOH tolerance. CTA1 and longevity are primer systems promoting phenotype-specific gene expression. The lower cell viability and growth under stress is a byproduct of sphingolipids and inositol phosphorylceramide dampening, acerbated in HTs by sphinganine, ERG9, and squalene overloads; LTs diminish this harm by accumulating inositol 1-phosphate. The diauxic shift drives an EtOH buffering by promoting an energy burst under stress, mainly in HTs. Analysis of mutants showed genes and lncRNAs in three strains critical for their EtOH tolerance. Finally, longevity, peroxisome, energy and lipid metabolisms, RNA/protein degradation and storage systems are the main pathways driving the EtOH tolerance phenotypes.

systems biology↗