Disruption of the mitogen-activated protein kinase pathway, MEKK1-MKK1/MKK2-MPK4 (hereafter designated as MEKK1 pathway), leads to the activation of distinct NLRs (nucleotide-binding and leucine-rich repeat receptors), TNL (TIR-type NLR) SMN1, and CNL (CC-type NLR) SUMM2, resulting in dwarf and autoimmune phenotypes. Unlike and mutants, the dwarf and autoimmune phenotypes of are only partially suppressed by the mutation, suggesting a significant contribution of to the phenotypes. However, full suppression of by the double mutation remains to be elucidated. To address this key question, we generated a triple mutant and analyzed the dwarf and constitutive cell death phenotypes. The triple mutant showed restoration of plant size with no detectable cell death, indicating full suppression of the dwarf and autoimmune phenotypes. These results suggest that SMN1 and SUMM2 constitute a robust surveillance system for the MEKK1 pathway against pathogen infection.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8973378 | PMC |
http://dx.doi.org/10.1080/15592324.2022.2046412 | DOI Listing |
Plant Physiol
December 2024
State Key Laboratory of Plant Environmental Resilience, College of Life Sciences, Zhejiang University, Hangzhou, Zhejiang 310058, China.
Two mitogen-activated protein kinase (MAPK) cascades with MPK4 and MPK3/MPK6 as the bottommost kinases are key to plant growth/development and immune signaling. Disruption of the MPK4 cascade leads to severe dwarfism and autoimmunity, complicating the study of MPK4 in plant growth/development and immunity. In this study, we successfully rescued the Arabidopsis (Arabidopsis thaliana) mpk4 mutant using a chemical-sensitized MPK4 variant, MPK4YG, creating a conditional activity-null mpk4 mutant named MPK4SR (genotype: PMPK4:MPK4YG mpk4) that could be used to examine the functions of MPK4 in plant growth/development and immunity.
View Article and Find Full Text PDFAllergol Select
October 2024
Center for Child and Adolescent Health, Helios Hospital Krefeld, Academic Hospital of RWTH Aachen, Krefeld.
Nat Plants
September 2024
Department of Biology, Duke University, Durham, NC, USA.
Over the past three decades, researchers have isolated plant mutants that show constitutively activated defence responses in the absence of pathogen infection. These mutants are called autoimmune mutants and are typically dwarf and/or bearing chlorotic/necrotic lesions. Here, from a genetic screen for Arabidopsis genes involved in maintaining a normal leaf microbiota, we identified TIP GROWTH DEFECTIVE 1 (TIP1), which encodes an S-acyltransferase, as a key player in guarding leaves against abnormal microbiota level and composition under high-humidity conditions.
View Article and Find Full Text PDFClin Endocrinol (Oxf)
September 2024
Newcastle University and Great North Children's Hospital, Newcastle upon Tyne, UK.
The spectrum of thyroid disorders presenting to paediatricians is different to that seen by adult physicians. Referrals reflect cases detected by the neonatal screening programme for congenital hypothyroidism and many of the inherited defects of thyroid hormone generation or action will be manifest in early life. Autoimmune thyroid disease can be particularly challenging to manage in the young and the potential impact of thyroid status on neurodevelopment and schooling are key considerations throughout childhood and adolescence.
View Article and Find Full Text PDFJCO Clin Cancer Inform
January 2024
Department of Biology, Howard University, Washington, DC.
Purpose: Thyroid peroxidase (TPO) is essential for the synthesis of thyroid hormones. However, specific mutations render TPO antigenic and prone to autoimmune attacks leading to thyroid cancer, TPO deficiency, and congenital hypothyroidism (CH). Despite technological advancement, most experimental procedures cannot quickly identify the genetic causes of CH nor detect thyroid cancer in the early stages.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!