Abstract

The intracellular infection thread initiated in a root hair cell is a unique structure associated with Rhizobium-legume symbiosis. It is characterized by inverted tip growth of the plant cell wall, resulting in a tunnel that allows invasion of host cells by bacteria during the formation of the nitrogen-fixing root nodule. Regulation of the plant-microbial interface is essential for infection thread growth. This involves targeted deposition of the cell wall and extracellular matrix and tight control of cell wall remodeling. This review describes the potential role of different actors such as transcription factors, receptors, and enzymes in the rearrangement of the plant-microbial interface and control of polar infection thread growth. It also focuses on the composition of the main polymers of the infection thread wall and matrix and the participation of reactive oxygen species (ROS) in the development of the infection thread. Mutant analysis has helped to gain insight into the development of host defense reactions. The available data raise many new questions about the structure, function, and development of infection threads.

Highlights

  • This involves targeted deposition of the cell wall and extracellular matrix and tight control of cell wall remodeling

  • In P. sativum plants, the RG‐II complex with boron and Arabinogalactan protein‐extensins protein-extensins (AGPEs) was observed in the infection thread matrix, while the rhizobial cells were separated from the matrix by Borate is an essential micronutrient for legume nodule development

  • Infection threads represent a third type of tip growth for the deposition of cell wall material

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Summary

Introduction

During the course of evolution, plants have exploited certain properties of microorganisms to expand their functional capabilities. In the case of intercellular invasion, rhizobia can penetrate into the host tissue by several different routes: through the middle lamellae between adjacent root hair cells; through wounds arising during lateral root appearance (‘crack entry’); and directly between cells of the intact epidermis [7,8,9,10,11] In this case, the subsequent colonization of the nodule primordium occurs as a result of intercellular infection, which is accompanied by the formation of tubular intercellular structures that resemble intracellular infection. We will explore the sequential development of the symbiotic interface, which involves the remodeling of the cell wall and extracellular matrix during the growth of infection threads This process stretches from the early stages of tissue invasion in root hairs through to the stage when biological nitrogen fixation develops within the host cells of mature nodules

Molecular Dialogue
Attachment of Rhizobia
Curling of Root Hairs
Initiation of the Infection Thread
The Nodule Primordium and Nodule Meristem
Propagation of the Infection Thread
Infection infection thread in in thethe nodules of Figure
Infection Thread Wall
Enzymes Involved in the Growth of the Infection Thread
Polysaccharides and Proteins of the Infection Thread Wall
Infection Thread Matrix
Arabinogalactan
Sequential
Defense Reactions
Release of Bacteria from Infection Threads
Nodule Senescence and Release of Bacteria
Environmental Influences
Conclusions and Perspectives
Structure and development of the interface in infection
Findings
O2 plays athe role ina cross-linking of AGPEs and cross‐linking
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