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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.

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