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Transcriptomic evidence for distinct mechanisms underlying abscission deficiency in the Arabidopsis mutants haesa/haesa-like 2 and nevershed.

ABSTRACT: OBJECTIVE:In Arabidopsis, the abscission of floral organs is regulated by two related receptor-like protein kinases, HAESA and HAESA-like 2 (HAE/HSL2). Signaling by HAE/HSL2 leads to expression of genes encoding secreted cell wall remodeling and hydrolase enzymes. hae hsl2 mutants fail to induce expression of these genes and retain floral organs indefinitely. Mutants in the gene NEVERSHED (NEV) also fail to abscise floral organs and phenotypically resemble hae hsl2. NEV encodes an ADP-ribosylation factor GTPase-activating protein that localizes to the trans-Golgi network and early endosome. nev displays altered Golgi morphology and aberrations in vesicular trafficking. The mechanism by which nev fails to abscise is presently unknown. It has been hypothesized that nev fails to activate HAE/HSL2 signaling. In this study we use RNA-Sequencing to test this hypothesis. RESULTS:We show that the transcriptional alterations in hae hsl2 and nev are highly divergent. hae hsl2 displays a clear reduction in expression of genes associated with cell wall remodeling and pectin degradation, while nev displays vast transcriptional changes associated with response to pathogens. These results suggest that the mechanism of the defect between hae hsl2 and nev are distinct.

SUBMITTER: Taylor I

PROVIDER: S-EPMC6199728 | biostudies-literature | 2018 Oct

REPOSITORIES: biostudies-literature

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Transcriptomic evidence for distinct mechanisms underlying abscission deficiency in the Arabidopsis mutants haesa/haesa-like 2 and nevershed.

Taylor Isaiah I Walker John C JC

BMC research notes 20181023 1

<h4>Objective</h4>In Arabidopsis, the abscission of floral organs is regulated by two related receptor-like protein kinases, HAESA and HAESA-like 2 (HAE/HSL2). Signaling by HAE/HSL2 leads to expression of genes encoding secreted cell wall remodeling and hydrolase enzymes. hae hsl2 mutants fail to induce expression of these genes and retain floral organs indefinitely. Mutants in the gene NEVERSHED (NEV) also fail to abscise floral organs and phenotypically resemble hae hsl2. NEV encodes an ADP-ri ...[more]

PMID: 30352616

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Project description:BackgroundAbscission is an active, organized, and highly coordinated cell separation process enabling the detachment of aerial organs through the modification of cell-to-cell adhesion and breakdown of cell walls at specific sites on the plant body known as abscission zones. In Arabidopsis thaliana, abscission of floral organs and cauline leaves is regulated by the interaction of the hormonal peptide INFLORESCENCE DEFICIENT IN ABSCISSION (IDA), a pair of redundant receptor-like protein kinases, HAESA (HAE) and HAESA-LIKE2 (HSL2), and SOMATIC EMBRYOGENESIS RECEPTOR-LIKE KINASE (SERK) co-receptors. However, the functionality of this abscission signaling module has not yet been demonstrated in other plant species.ResultsThe expression of the pair of NbenIDA1 homeologs and the receptor NbenHAE.1 was supressed at the base of the corolla tube by the inoculation of two virus-induced gene silencing (VIGS) constructs in Nicotiana benthamiana. These gene suppression events arrested corolla abscission but did not produce any obvious effect on plant growth. VIGS plants retained a higher number of corollas attached to the flowers than control plants, an observation related to a greater corolla breakstrength. The arrest of corolla abscission was associated with the preservation of the parenchyma tissue at the base of the corolla tube that, in contrast, was virtually collapsed in normal corollas. In contrast, the inoculation of a viral vector construct that increased the expression of NbenIDA1A at the base of the corolla tube negatively affected the growth of the inoculated plants accelerating the timing of both corolla senescence and abscission. However, the heterologous ectopic overexpression of citrus CitIDA3 and Arabidopsis AtIDA in N. benthamiana did not alter the standard plant phenotype suggesting that the proteolytic processing machinery was unable to yield active peptides.ConclusionHere, we demonstrate that the pair of NbenIDA1 homeologs encoding small peptides of the IDA-like family and the receptor NbenHAE.1 control cellular breakdown at the base of the corolla tube awhere an adventitious AZ should be formed and, therefore, corolla abscission in N. benthamiana flowers. Altogether, our results provide the first evidence supporting the notion that the IDA-HAE/HSL2 signaling module is conserved in angiosperms.

Project description:Over the past decade, large-scale genetic studies have successfully identified hundreds of genetic variants robustly associated with risk for psychiatric disorders. However, mechanistic insight and clinical translation continue to lag the pace of risk variant identification, hindered by the sheer number of targets and their predominant noncoding localization, as well as pervasive pleiotropy and incomplete penetrance. Successful next steps require identification of "causal" genetic variants and their proximal biological consequences; placing variants within biologically defined functional contexts, reflecting specific molecular pathways, cell types, circuits, and developmental windows; and characterizing the downstream, convergent neurobiological impact of polygenicity within an individual. Here, we discuss opportunities and challenges of high-throughput transcriptomic profiling in the human brain, and how transcriptomic approaches can help pinpoint mechanisms underlying genetic risk for psychiatric disorders at a scale necessary to tackle daunting levels of polygenicity. These include transcriptome-wide association studies for risk gene prioritization through integration of genome-wide association studies with expression quantitative trait loci. We outline transcriptomic results that inform our understanding of the brain-level molecular pathology of psychiatric disorders, including autism spectrum disorder, bipolar disorder, major depressive disorder, and schizophrenia. Finally, we discuss systems-level approaches for integration of distinct genetic, genomic, and phenotypic levels, including combining spatially resolved gene expression and human neuroimaging maps. Results highlight the importance of understanding gene expression (dys)regulation across human brain development as a major contributor to psychiatric disease pathogenesis, from common variants acting as expression quantitative trait loci to rare variants enriched for gene expression regulatory pathways.

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Transcriptomic evidence for distinct mechanisms underlying abscission deficiency in the Arabidopsis mutants haesa/haesa-like 2 and nevershed.

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Transcriptomic evidence for distinct mechanisms underlying abscission deficiency in the Arabidopsis mutants haesa/haesa-like 2 and nevershed.

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