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

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 ex...

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Detalles Bibliográficos
Autores principales: Taylor, Isaiah, Walker, John C.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6199728/
https://www.ncbi.nlm.nih.gov/pubmed/30352616
http://dx.doi.org/10.1186/s13104-018-3864-x
Descripción
Sumario: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. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s13104-018-3864-x) contains supplementary material, which is available to authorized users.