KLF5 ChIP-seq in CP-A and OE19 cells
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Illumina HiSeq 4000
ORGANISM(S): Homo sapiens
SUBMITTER: Connor Rogerson
PROVIDER: E-MTAB-8568 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:KLF5 ChIP-seq in CP-A and OE19 cells
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Project description:The past twenty years have seen tremendous advances in our understanding of the mechanisms underlying bacterial cytokinesis, particularly the composition of the division machinery and the factors controlling its assembly. At the same time, however, we understand very little about the relationship between cell division and other cell cycle events in bacteria. Here we report that inhibiting division in Bacillus subtilis and Staphylococcus aureus quickly leads to an arrest in the initiation of new rounds of DNA replication followed by a complete arrest in cell growth. Arrested cells are metabolically active but unable to initiate new rounds of either DNA replication or division when shifted to permissive conditions. Inhibiting DNA replication results in entry into a similar quiescent state, in which cells are unable to resume growth or division when returned to permissive conditions. Our findings suggest the presence of two cell cycle control points: one linking division to the initiation of DNA replication and another linking the initiation of DNA replication to division. Significantly, this evidence contradicts the prevailing view of the bacterial cell cycle as a series of coordinated but uncoupled events. Importantly, the terminal nature of the cell cycle arrest validates the bacterial cell cycle machinery as an effective target for antimicrobial development. Four-condition experiment: ftsZ induced for 1hr, ftsZ depleted for 1hr, ftsZ induced for 2hrs, ftsZ depleted for 2hrs. Biological replicates: 3-4 for each sample. Reference: a mixture of wt RNA from different growth phases and wt backgrounds.
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