Dataset Information

Respiratory Burst Oxidase Homolog D as a Modulating Component of Oxidative Response under Ammonium Toxicity.

ABSTRACT: Delayed growth, a visible phenotypic component of the so-called ammonium syndrome, occurs when ammonium is the sole inorganic nitrogen source. Previously, we have shown that modification of apoplastic reactive oxygen species (apROS) metabolism is a key factor contributing to plant growth retardation under ammonium nutrition. Here, we further analyzed the changes in apROS metabolism in transgenic plants with disruption of the D isoform of the respiratory burst oxidase homolog (RBOH) that is responsible for apROS production. Ammonium-grown Arabidopsisrbohd plants are characterized by up to 50% lower contents of apoplastic superoxide and hydrogen peroxide. apROS sensing markers such as OZF1 and AIR12 were downregulated, and the ROS-responsive signaling pathway, including MPK3, was also downregulated in rbohd plants cultivated using ammonium as the sole nitrogen source. Additionally, the expression of the cell-wall-integrity marker FER and peroxidases 33 and 34 was decreased. These modifications may contribute to phenomenon wherein ammonium inhibited the growth of transgenic plants to a greater extent than that of wild-type plants. Overall, this study indicated that due to disruption of apROS metabolism, rbohd plants cannot adjust to ammonium toxicity and are more sensitive to these conditions.

SUBMITTER: Burian M

PROVIDER: S-EPMC9031508 | biostudies-literature | 2022 Apr

REPOSITORIES: biostudies-literature

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Respiratory Burst Oxidase Homolog D as a Modulating Component of Oxidative Response under Ammonium Toxicity.

Burian Maria M Podgórska Anna A Ostaszewska-Bugajska Monika M Szal Bożena B

Antioxidants (Basel, Switzerland) 20220402 4

Delayed growth, a visible phenotypic component of the so-called ammonium syndrome, occurs when ammonium is the sole inorganic nitrogen source. Previously, we have shown that modification of apoplastic reactive oxygen species (apROS) metabolism is a key factor contributing to plant growth retardation under ammonium nutrition. Here, we further analyzed the changes in apROS metabolism in transgenic plants with disruption of the D isoform of the respiratory burst oxidase homolog (RBOH) that is respo ...[more]

PMID: 35453389

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Project description:Verticillium wilt, mainly caused by a soil-inhabiting fungus Verticillium dahliae, can seriously reduce the yield and quality of cotton. The complex mechanism underlying cotton resistance to Verticillium wilt remains largely unknown. In plants, reactive oxygen species (ROS) mediated by Rbohs is one of the earliest responses of plants to biotic and abiotic stresses. In our previous study, we performed a time-course phospho-proteomic analysis of roots of resistant and susceptible cotton varieties in response to V. dahliae, and found early differentially expressed protein burst oxidase homolog protein D (GhRbohD). However, the role of GhRbohD-mediated ROS in cotton defense against V. dahliae needs further investigation. In this study, we analyzed the function of GhRbohD-mediated resistance of cotton against V. dahliae in vitro and in vivo. Bioinformatics analysis showed that GhRbohD possessed the conservative structural attributes of Rbohs family, 12 members of RbohD out of 57 Rbohs in cotton. The expression of GhRbohD was significantly upregulated after V. dahliae inoculation, peaking at 6 hpi, and the phosphorylation level was also increased. A VIGS test demonstrated that ROS production, NO, H2O2 and Ca2+ contents of GhRbohD-silenced cotton plants were significantly reduced, and lignin synthesis and callose accumulation were damaged, important reasons for the impairment of GhRbohD-silenced cotton's defense against V. dahliae. The expression levels of resistance-related genes were downregulated in GhRbohD-silenced cotton by qRT-PCR, mainly involving the lignin metabolism pathway and the jasmonic acid signaling pathway. However, overexpression of GhRbohD enhanced resistance of transgenic Arabidopsis to V. dahliae challenge. Furthermore, Y2H assays were applied to find that GhPBL9 and GhRPL12C may interact with GhRbohD. These results strongly support that GhRbohD activates ROS production to positively regulate the resistance of plants against V. dahliae.

Dataset Information

Respiratory Burst Oxidase Homolog D as a Modulating Component of Oxidative Response under Ammonium Toxicity.

Publications

Respiratory Burst Oxidase Homolog D as a Modulating Component of Oxidative Response under Ammonium Toxicity.

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