Endopolyploidization and flowering time are antagonistically regulated by checkpoint component MAD1 and immunity modulator MOS1

Bao, Zhiyi; Zhang, Ning; Hua, Jian

doi:10.1038/ncomms6628

Cited by 43 publications

(61 citation statements)

References 53 publications

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“…The bon1 mos1 smo1 plants, along with Col-0, bon1 and bon1 mos1, were infected by the virulent pathogen Pst DC3000. Consistent with a previous study (Bao et al, 2014), pathogens grew significantly less in bon1 compared to Col-0 and bon1 mos1 had more pathogen growth compared to bon1 (Fig. 1b).…”

Section: Resultssupporting

confidence: 92%

HOS15 and HDA9 negatively regulate immunity through histone deacetylation of intracellular immune receptor NLR genes in Arabidopsis

et al. 2020

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Summary Plant immune responses need to be tightly controlled for growth–defense balance. The mechanism underlying this tight control is not fully understood. Here we identify epigenetic regulation of nucleotide‐binding leucine rich repeat or Nod‐Like Receptor (NLR) genes as an important mechanism for immune responses. Through a sensitized genetic screen and molecular studies, we identified and characterized HOS15 and its associated protein HDA9 as negative regulators of immunity and NLR gene expression. The loss‐of‐function of HOS15 or HDA9 confers enhanced resistance to pathogen infection accompanied with increased expression of one‐third of the 207 NLR genes in Arabidopsis thaliana. HOS15 and HDA9 are physically associated with some of these NLR genes and repress their expression likely through reducing the acetylation of H3K9 at these loci. In addition, these NLR genes are repressed by HOS15 under both pathogenic and nonpathogenic conditions but by HDA9 only under infection condition. Together, this study uncovers a previously uncharacterized histone deacetylase complex in plant immunity and highlights the importance of epigenetic regulation of NLR genes in modulating growth–defense balance.

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Section: Resultssupporting

confidence: 92%

HOS15 and HDA9 negatively regulate immunity through histone deacetylation of intracellular immune receptor NLR genes in Arabidopsis

et al. 2020

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“…In contrast, expressions of CYCD3 ; 1 and CDC20 . 1 were reduced by 42% and 36% respectively in mos1 compared with the wild‐type (Figure a; Bao et al ., ). These data indicate that the expression of some cell‐cycle genes is altered in mos1 .…”

Section: Resultsmentioning

confidence: 97%

“…Another factor that modulates both cell cycle and plant immunity is MOS1 (MODIFIER OF snc1-1). MOS1 is essential for the upregulation of a NLR gene SNC1 in the autoimmune mutants snc1 and bonzai1 (bon1) (Li et al, 2010a, b;Bao et al, 2014). It does not appear to affect SNC1 expression through altering DNA methylation, but its regulation was postulated to be involved in chromatin modification (Li et al, 2010a(Li et al, , b, 2011.…”

Section: Introductionmentioning

confidence: 99%

“…It does not appear to affect SNC1 expression through altering DNA methylation, but its regulation was postulated to be involved in chromatin modification (Li et al, 2010a(Li et al, , b, 2011. MOS1 has also been found to regulate endoreduplication and flowering time and its loss of function (LOF) mutant is late flowering and has increased endoreduplication (Bao et al, 2014). Intriguingly, this role of MOS1 is antagonized by Mitotic Arrest Deficient 1 (MAD1) encoding a component of spindle assembly checkpoint complex (SAC) (Bao et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

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MOS1 functions closely with TCP transcription factors to modulate immunity and cell cycle in Arabidopsis

et al. 2017

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These authors contributed equally to this work. SUMMARYEmerging evidence indicates a close connection between cell-cycle progression and the plant immune responses. In Arabidopsis, MODIFIER OF snc1-1 (MOS1) modulates a number of processes including endoreduplication and plant disease resistance, but the molecular mechanism underlying this modulation was not fully understood. Here, we provide biochemical and genetic evidence that TEOSINTE BRANCHED 1, CYCLOIDEA, PCF1 (TCP) transcription factors TCP15 and its homologues are mediators of MOS1 function in the immune response and are likely to be also involved in cell-cycle control. MOS1 and TCP proteins have a direct physical interaction. They both bind to the promoter of the immune receptor gene SUPRESSOR OF npr1-1, CONSTITUTIVE 1 (SNC1) and modulate its expression and consequently immune responses. MOS1 and TCP15 both affect the expression of cell-cycle genes D-type CYCLIN 3;1 (CYCD3;1), which may mediate the MOS1 function in cell-cycle modulation. In addition, CYCD3;1 overexpression upregulates immune responses, and SNC1 expression. This study investigated and revealed a role for MOS1 in transcriptional regulation through TCP15 and its homologues. This finding suggests the coordination of cell-cycle progression and plant immune responses at multiple levels.

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“…Additionally, we also identify novel temperature-induced splicing events in master regulators of various biological processes, such as the flowering time regulator SQUAMOSA PROMOTER BINDING PROTEIN-LIKE 2 ( SPL2 ) [36] and MODIFIER OF SNC 1 ( MOS1 ) [37], the regulators of auxin signaling AUXIN RESPONSE FACTOR 2 ( ARF2 ) [38] and PIN-FORMED 7 ( PIN7 ) [39], and the chromatin remodelers VIN3-LIKE 2 ( VIL2 ) [40] and SPLAYED ( SYD ) [41–43] (Fig. 1b and Additional file 1: Table S1).…”

Section: Resultsmentioning

confidence: 99%

Histone H3 lysine 36 methylation affects temperature-induced alternative splicing and flowering in plants

et al. 2017

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Background: Global warming severely affects flowering time and reproductive success of plants. Alternative splicing of pre-messenger RNA (mRNA) is an important mechanism underlying ambient temperature-controlled responses in plants, yet its regulation is poorly understood. An increase in temperature promotes changes in plant morphology as well as the transition from the vegetative to the reproductive phase in Arabidopsis thaliana via changes in splicing of key regulatory genes. Here we investigate whether a particular histone modification affects ambient temperature-induced alternative splicing and flowering time.Results: We use a genome-wide approach and perform RNA-sequencing (RNA-seq) analyses and histone H3 lysine 36 tri-methylation (H3K36me3) chromatin immunoprecipitation sequencing (ChIP-seq) in plants exposed to different ambient temperatures. Analysis and comparison of these datasets reveal that temperature-induced differentially spliced genes are enriched in H3K36me3. Moreover, we find that reduction of H3K36me3 deposition causes alteration in temperature-induced alternative splicing. We also show that plants with mutations in H3K36me3 writers, eraser, or readers have altered high ambient temperature-induced flowering. Conclusions: Our results show a key role for the histone mark H3K36me3 in splicing regulation and plant plasticity to fluctuating ambient temperature. Our findings open new perspectives for the breeding of crops that can better cope with environmental changes due to climate change.

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Endopolyploidization and flowering time are antagonistically regulated by checkpoint component MAD1 and immunity modulator MOS1

Cited by 43 publications

References 53 publications

HOS15 and HDA9 negatively regulate immunity through histone deacetylation of intracellular immune receptor NLR genes in Arabidopsis

HOS15 and HDA9 negatively regulate immunity through histone deacetylation of intracellular immune receptor NLR genes in Arabidopsis

MOS1 functions closely with TCP transcription factors to modulate immunity and cell cycle in Arabidopsis

Histone H3 lysine 36 methylation affects temperature-induced alternative splicing and flowering in plants

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