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

. 2023 Nov 28;223(2):e202211026. doi: 10.1083/jcb.202211026

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

© 2023 Mahone et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/).

PMC Copyright notice

Figure 10. — FzlA binds to FtsZ and signals through FtsK to shift FtsW to a slow-moving, active state. (A) When FtsK is actively segregating chromosomal termini from the division plane, it has limited interaction with FzlA and signaling downstream to activate FtsWI does not occur. Inactive FtsW molecules either move with FtsZ clusters as they treadmill about the division plane or are stationary. FzlA molecules treadmill with FtsZ or remain stationary. (B) When FtsK is not bound to DNA, the FzlA C-terminal tail can bind to FtsK_C to signal downstream for FtsWI activation, thereby coupling chromosome segregation to constriction progression. (A and B) Black arrows indicate hypothesized signaling. Green arrows indicate direct interactions confirmed in Caulobacter. Other divisome components depicted for hypothesized downstream interactions: A, FtsA; QLB, FtsQLB complex; N, FtsN.