Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2020 Feb 10;11:816. doi: 10.1038/s41467-020-14585-6

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

Fig. 5 — a Model of ShkA-TacA phosphorelay activation and its contribution to G1/S transition. The upper part shows the intercalated network of kinases (PleC, DivJ, ShkA, CckA) and response regulators (PleD, TacA, DivK) that contribute to G1/S transition. HK indicates a hypothetical histidine kinase that controls the activity of PleD and possibly DivK (stippled lines) and by that acts as kick-starter for G1 exit. HK expression is postulated to be CtrA-mediated (stippled line). The initial, HK-PleD-mediated increase of c-di-GMP activates the ShkA-TacA pathway, resulting in a SpmX-DivJ-PleD-mediated further boost of c-di-GMP concentration, which activates the CckA phosphatase and PopA. Note that ShkA has a five- to tenfold higher affinity for c-di-GMP compared with CckA and PopA. The block of replication initiation by binding of activated CtrA to the chromosomal origin of replication (Cori) is indicated. The lower part of the graph indicates time windows of CckA kinase and phosphatase as well as TacA kinase activity. The gradual increase of c-di-GMP during G1/S is indicated. b Activity of the spmX promoter in strains harboring a spmX’-‘lacZ reporter fusion (pAK502-spmX). Shown are mean values and standard deviations (N = 3). c Activity of the tacA promoter in strains harboring a tacA’-‘lacZ fusion (pAK502-tacA). Strains with a chromosomal pleC deletion express wild type and mutant pleC alleles from plasmid pQF under control of their native promoter. PleC(F778L): Kinase−/phosphatase+ (K−P+); PleC(T614R) kinase−/phosphatase− (K−P−); - indicates the empty vector control (plasmid pQF). Shown are mean values and standard deviations (N = 3). d Immunoblots of selected strains shown in c probed with anti-SpmX and anti-MreB antibodies (top) or anti-PleC antibodies (bottom). e Immunoblots of selected strains shown in c probed with anti-SpmX and anti-MreB antibodies. f Immunoblots of indicated strains probed with anti-SpmX and anti-MreB antibodies. pPleD* indicates a pMR20-based plasmid (pPA114-47) expressing the constitutively active, phosphorylation-independent PleD* allele. EV denotes the empty plasmid control (pMR20). Source data are provided as a Source Data file.