MOS2 has redundant function with its homolog MOS2H and is required for proper splicing of<i>SNC1</i>

Copeland, Charles; Xu, Shaohua; Qi, Yijun; Li, Xin

doi:10.4161/psb.25372

Cited by 14 publications

(8 citation statements)

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“…To identify negative regulators of NLR mediated immunity we performed a snc1 enhancer screen using both mos2 snc1 npr1 and mos4 snc1 backgrounds (Huang et al ., ) to search for mutants that restore or enhance snc1 ‐like morphology and constitutive defense responses despite the suppressive effects of mos2 or mos4 . As MOS2 and MOS4 are involved in RNA processing and contribute to proper splicing of SNC1 (Zhang et al ., ; Palma et al ., ; Xu et al ., ; Copeland et al ., ), loss of this regulation in mos2 or mos4 mutants suppresses the constitutive immune responses observed in snc1 plants. Our screen resulted in the isolation of over 10 mutant, snc1‐enhancing ( muse ) mutants (Huang et al ., ), including muse10 and muse12 which were isolated in the mos2 snc1 npr1 background.…”

Section: Resultsmentioning

confidence: 99%

HSP90s are required for NLR immune receptor accumulation in Arabidopsis

et al. 2014

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SUMMARYHeat shock proteins (HSPs) serve as molecular chaperones for diverse client proteins in many biological processes. In plant immunity, cytosolic HSP90s participate in the assembly, stability control and/or activation of immune receptor complexes. In this paper we report that in addition to the well-established positive roles that HSP90 isoforms play in plant immunity, they are also involved in the negative regulation of immune receptor accumulation. Point mutations in two HSP90 genes, HSP90.2 and HSP90.3, were identified from a forward genetic screen designed to isolate mutants with enhanced disease resistance. We found that specific mutations in HSP90.2 and HSP90.3 lead to heightened accumulation of immune receptors, including SNC1, RPS2 and RPS4. HSP90s may assist SGT1 in the formation of SCF E3 ubiquitin ligase complexes that target immune receptors for degradation. Such regulation is critical for maintaining appropriate levels of immune receptor proteins to avoid autoimmunity.

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Section: Resultsmentioning

confidence: 99%

HSP90s are required for NLR immune receptor accumulation in Arabidopsis

et al. 2014

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“…Splicing defects in both pri-miRNAs and pre-mRNAs were detected in abh1/cbp80, cbp20, sic-1 and sta1-1 mutants (Laubinger et al ., 2008; reviewed in Gonatopoulos-Pournatzis & Cowling, 2014). AtGRP7 overexpression results in changes in pri-miRNA splicing (Streitner et al ., 2012; Koster et al ., 2014) MOS2 is required for appropriate splicing of SNC1 ( SUPPRESSOR OF NPR1-1, CONSTITUTIVE 1 ), which encodes a Toll Interleukin 1 Receptor Nucleotide Binding Leucine-Rich Repeat (TIR-NB-LRR) class of protein involved in plant defense responses (Zhang et al ., 2005; Copeland et al ., 2013). Alternatively spliced SR gene transcripts were detected in tho1 and tho2 mutants (Furumizu et al ., 2010; Francisco-Mangilet et al ., 2015).…”

Section: Microrna Biogenesis In Plantsmentioning

confidence: 99%

The ‘how’ and ‘where’ of plant microRNAs

2017

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Contents 1002I.1002II.1007III.1010IV.10131013References1013 Summary MicroRNAs (miRNAs) are small non‐coding RNAs, of typically 20–24 nt, that regulate gene expression post‐transcriptionally through sequence complementarity. Since the identification of the first miRNA, lin‐4, in the nematode Caenorhabditis elegans in 1993, thousands of miRNAs have been discovered in animals and plants, and their regulatory roles in numerous biological processes have been uncovered. In plants, research efforts have established the major molecular framework of miRNA biogenesis and modes of action, and are beginning to elucidate the mechanisms of miRNA degradation. Studies have implicated restricted and surprising subcellular locations in which miRNA biogenesis or activity takes place. In this article, we summarize the current knowledge on how plant miRNAs are made and degraded, and how they repress target gene expression. We discuss not only the players involved in these processes, but also the subcellular sites in which these processes are known or implicated to take place. We hope to raise awareness that the cell biology of miRNAs holds the key to a full understanding of these enigmatic molecules.

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“…A previous forward genetic screen for suppressors of snc1, called the Modifier of snc1 (MOS) screen, identified a number of positive regulators of NLR-mediated immunity, including MOS2. Through affecting the splicing pattern of SNC1, the mos2 mutation suppresses the autoimmune phenotype of snc1, resulting in larger plant size, reduced defense marker PR gene expression, and disease susceptibility to the oomycete pathogen Hyaloperonospora arabidopsidis Noco2 (Zhang et al, 2005;Copeland et al, 2013). In order to identify novel negative regulators of NLR-mediated immunity, modified snc1 enhancer screens were carried out in snc1 mos backgrounds (Huang et al, 2013).…”

Section: Identification and Characterization Of The Muse8 Snc1 Mos2 Nmentioning

confidence: 99%

AtCDC48A is involved in the turnover of an NLR immune receptor

et al. 2016

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Plants rely on different immune receptors to recognize pathogens and defend against pathogen attacks. Nucleotide-binding domain and leucine-rich repeat (NLR) proteins play a major role as intracellular immune receptors. Their homeostasis must be maintained at optimal levels in order to effectively recognize pathogens without causing autoimmunity. Previous studies have shown that the activity of the ubiquitin-proteasome system is essential to prevent excessive accumulation of NLR proteins such as Suppressor of NPR1, Constitutive 1 (SNC1). Attenuation of the ubiquitin E3 ligase SCF (Constitutive expressor of Pathogenesis Related genes 1) or the E4 protein MUSE3 (Mutant, SNC1-Enhancing 3) leads to NLR accumulation and autoimmunity. In the current study, we report the identification of AtCDC48A as a negative regulator of NLR-mediated immunity. Plants carrying Atcdc48A-4, a partial loss-of-function allele of AtCDC48A, exhibit dwarf morphology and enhanced disease resistance to the oomycete pathogen Hyaloperonospora arabidopsidis (H.a.) Noco2. The SNC1 level is increased in Atcdc48A-4 plants and AtCDC48A interacts with MUSE3 in co-immunoprecipitation experiments, supporting a role for AtCDC48A in NLR turnover. While Arabidopsis contains four other paralogs of AtCDC48A, knockout mutants of these genes do not show obvious immunity-related phenotypes, suggesting functional divergence within this family. As an AAA-ATPase, AtCDC48A likely serves to process the poly-ubiquitinated NLR substrate for final protein degradation by the 26S proteasome.

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MOS2 has redundant function with its homolog MOS2H and is required for proper splicing ofSNC1

Cited by 14 publications

References 14 publications

HSP90s are required for NLR immune receptor accumulation in Arabidopsis

HSP90s are required for NLR immune receptor accumulation in Arabidopsis

The ‘how’ and ‘where’ of plant microRNAs

AtCDC48A is involved in the turnover of an NLR immune receptor

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