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

. 2021 Jan 21;11:2034. doi: 10.1038/s41598-021-81598-6

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

© The Author(s) 2021

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

Proposed model for nodulation signaling and modulation by Bradryhizobium elkanii type III effector Bel2-5. A soybean root-derived genistein induces the production of Nod factors (NFs) in B. elkanii. Recognition of NFs by NF receptors triggers a signaling cascade leading to nodulation. The genistein also induces B. elkanii to inject effector proteins into soybean cells. NopL suppress plant defense responses by modulating the MAPK cascade. The ErnA effector triggers nodule organogenesis by a yet unknown mechanism. Bel2-5 effector likely interferes with the nodulation signaling pathway at least at two levels: (1) by modulating cytokinin biosynthesis-related genes that promoting nodule organogenesis and (2) by repressing ethylene biosynthesis-related genes and host-dependent defence responses that are deleterious to the bacterial infection. It should be noted that these DEGs may contain secondary and tertiary indirect effects as well as Bel2-5 direct effects.