{"doi":"10.1128/jb.00868-07","title":"DivL Performs Critical Cell Cycle Functions in<i>Caulobacter crescentus</i>Independent of Kinase Activity","abstract":"<jats:title>ABSTRACT</jats:title><jats:p>The<jats:italic>Caulobacter</jats:italic>cell cycle is regulated by a network of two-component signal transduction proteins. Phosphorylation and stability of the master transcriptional regulator CtrA are controlled by the CckA-ChpT phosphorelay, and CckA activity is modulated by another response regulator, DivK. In a screen to identify suppressors of the cold-sensitive<jats:italic>divK341</jats:italic>mutant, we found point mutations in the essential gene<jats:italic>divL</jats:italic>. DivL is similar to histidine kinases but has a tyrosine instead of a histidine at the conserved phosphorylation site (Y550). Surprisingly, we found that the ATPase domain of DivL is not essential for<jats:italic>Caulobacter</jats:italic>viability. We show that DivL selectively affects CtrA phosphorylation but not CtrA proteolysis, indicating that DivL acts in a pathway independent of the CckA-ChpT phosphorelay.<jats:italic>divL</jats:italic>can be deleted in a strain overproducing the phosphomimetic protein CtrAD51E, but unlike Δ<jats:italic>ctrA</jats:italic>cells expressing CtrAD51E, this strain is profoundly impaired in the control of chromosome replication and cell division. Thus, DivL performs a second function in addition to promoting CtrA phosphorylation. DivL is required for bipolar DivK localization and positively regulates DivK phosphorylation. Our results show that DivL controls two key cell cycle regulators, CtrA and DivK, and that phosphoryl transfer is not DivL's essential cellular activity.</jats:p>","journal":"Journal of Bacteriology","year":2007,"id":684291,"datarank":0.6010999777848708,"base_score":4.007333185232471,"endowment":4.007333185232471,"self_citation_contribution":0.6010999777848708,"citation_network_contribution":0.0,"self_endowment_contribution":0.6010999777848708,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":54,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":null,"is_data_producer":false,"deposit_databanks":null,"is_oa":false,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":null,"fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":1787667,"name":"Sarah Huntwork","orcid":null,"position":1,"is_corresponding":false},{"id":397487,"name":"Patrick H. Viollier","orcid":"0000-0002-5249-9910","position":2,"is_corresponding":false},{"id":890818,"name":"Kathleen R. Ryan","orcid":"0000-0003-3657-8069","position":3,"is_corresponding":false},{"id":1787665,"name":"Sarah J. Reisinger","orcid":null,"position":0,"is_corresponding":false}],"reference_count":0,"raw_metadata":{"has_enrichment":true,"resolved":true,"title":"DivL Performs Critical Cell Cycle Functions in<i>Caulobacter crescentus</i>Independent of Kinase Activity","abstract":"<jats:title>ABSTRACT</jats:title><jats:p>The<jats:italic>Caulobacter</jats:italic>cell cycle is regulated by a network of two-component signal transduction proteins. Phosphorylation and stability of the master transcriptional regulator CtrA are controlled by the CckA-ChpT phosphorelay, and CckA activity is modulated by another response regulator, DivK. In a screen to identify suppressors of the cold-sensitive<jats:italic>divK341</jats:italic>mutant, we found point mutations in the essential gene<jats:italic>divL</jats:italic>. DivL is similar to histidine kinases but has a tyrosine instead of a histidine at the conserved phosphorylation site (Y550). Surprisingly, we found that the ATPase domain of DivL is not essential for<jats:italic>Caulobacter</jats:italic>viability. We show that DivL selectively affects CtrA phosphorylation but not CtrA proteolysis, indicating that DivL acts in a pathway independent of the CckA-ChpT phosphorelay.<jats:italic>divL</jats:italic>can be deleted in a strain overproducing the phosphomimetic protein CtrAD51E, but unlike Δ<jats:italic>ctrA</jats:italic>cells expressing CtrAD51E, this strain is profoundly impaired in the control of chromosome replication and cell division. Thus, DivL performs a second function in addition to promoting CtrA phosphorylation. DivL is required for bipolar DivK localization and positively regulates DivK phosphorylation. Our results show that DivL controls two key cell cycle regulators, CtrA and DivK, and that phosphoryl transfer is not DivL's essential cellular activity.</jats:p>","is_dataset_classified":null,"base_score":4.007333185232471,"endowment":4.007333185232471,"datacite_reuse_total":0,"file_count":0,"downloads":0,"views":0,"has_version_chain":false,"is_dataset":false,"is_oa":false,"pmid":"17827294","pmcid":"PMC2168681","openalex_id":"https://openalex.org/W2127321623","authors":[],"funders":[{"funder_name":"NIGMS NIH HHS","grant_id":"R37 GM032506","title":null},{"funder_name":"NIGMS NIH HHS","grant_id":"GM032506","title":null},{"funder_name":"NIGMS NIH HHS","grant_id":"R01 GM032506","title":null}],"total_grants":3,"fwci":1.6993,"citation_percentile":0.82712488,"influential_citations":0,"citation_trend":[{"year":2012,"count":2},{"year":2013,"count":1},{"year":2014,"count":5},{"year":2015,"count":3},{"year":2016,"count":2},{"year":2017,"count":1},{"year":2018,"count":2},{"year":2019,"count":5},{"year":2020,"count":5},{"year":2021,"count":1},{"year":2022,"count":3},{"year":2023,"count":2},{"year":2025,"count":2}],"oa_status":"green","license":"https://journals.asm.org/non-commercial-tdm-license","oa_locations":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/2168681","host_type":"repository"},{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/2168681","host_type":"repository"},{"url":"https://journals.asm.org/doi/pdf/10.1128/JB.00868-07","host_type":"publisher"},{"url":"https://doi.org/10.1128/jb.00868-07","host_type":"journal"},{"url":"https://pubmed.ncbi.nlm.nih.gov/17827294","host_type":"repository"}],"fields_of_study":["Microtubule and mitosis dynamics","Cellular transport and secretion","Fungal and yeast genetics research","Alleles","Bacterial Proteins","Caulobacter crescentus","Cell Cycle","DNA-Binding Proteins","Gene Expression Regulation, Bacterial","Histidine Kinase","Mutation","Phosphorylation","Protein Kinases","Protein Transport","Transcription Factors"],"mesh_terms":["Histidine Kinase","Alleles","Bacterial Proteins","Cell Cycle","DNA-Binding Proteins","Mutation","Phosphorylation","Protein Kinases","Transcription Factors","Gene Expression Regulation, Bacterial","Caulobacter crescentus","Protein Transport"],"keywords":["Caulobacter crescentus","Biology","Cell biology","Cell cycle","Computational biology","Genetics","Cell"],"sdg_mappings":[],"linked_datasets":[],"clinical_trials":[],"software_tools":[],"database_accessions":[],"source":"live","citation_network_status":"fetched"},"created_at":"2026-08-18T13:44:04.077895Z","pmid":null,"pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}