The Arabidopsis DELAYED DEHISCENCE1 Gene Encodes an Enzyme in the Jasmonic Acid Synthesis Pathway

Abstract

delayed dehiscence1 is an Arabidopsis T-DNA mutant in which anthers release pollen grains too late for pollination to occur. The delayed dehiscence1 defect is caused by a delay in the stomium degeneration program. The gene disrupted in delayed dehiscence1 encodes 12-oxophytodienoate reductase, an enzyme in the jasmonic acid biosynthesis pathway. We rescued the mutant phenotype by exogenous application of jasmonic acid and obtained seed set from previously male-sterile plants. In situ hybridization studies showed that during the early stages of floral development, DELAYED DEHISCENCE1 mRNA accumulated within all floral organs. Later, DELAYED DEHISCENCE1 mRNA accumulated specifically within the pistil, petals, and stamen filaments. DELAYED DEHISCENCE1 mRNA was not detected in the stomium and septum cells of the anther that are involved in pollen release. The T-DNA insertion in delayed dehiscence1 eliminated both DELAYED DEHISCENCE1 mRNA accumulation and 12-oxophytodienoate reductase activity. These experiments suggest that jasmonic acid signaling plays a role in controlling the time of anther dehiscence within the flower.

High-resolution fine mapping of ps-2, a mutated gene conferring functional male sterility in tomato due to non-dehiscent anthers

“…In addition the sequence of the ps-2 gene will give us more insights into the physiology of anther dehiscence in tomato. Similar phenotypes have been observed in some Arabidopsis mutants where, in most of the cases, the jasmonic acid pathway was involved (Feys et al 1994;Ishiguro et al 2001;von Malek et al 2002;McConn and Browse 1996;Park et al 2002;Sanders et al 2000;Stintzi and Browse 2000;Xie et al 1998). Once the ps-2 gene is cloned, it will be interesting to know whether this gene is ortholog to one of those genes already identiWed in Arabidopsis.…”

“…The molecular mechanism of ps-2 in tomato is unknown, but similar mutant phenotypes have been observed and studied mainly in Arabidopsis, such as the mutant myb26 (Steiner-Lange et al 2003), the mutants coi1 (Feys et al 1994;Xie et al 1998) and dad1 (Ishiguro et al 2001), the double mutants opr3/ dde1 (Sanders et al 2000;Stintzi and Browse 2000) and aos/dde2-2 (von Malek et al 2002;Park et al 2002) and the triple mutant fad3/fad7/fad8 (McConn and Browse 1996). They are characterized by defects in Wlament elongation, timing of anther dehiscence and often show reduced pollen viability.…”

“…All, except the mutant myb26, are in one way or another involved in the jasmonic acid pathway. The mutant coi1 (Xie et al 1998) is insensitive to jasmonic acid, while the others are defective in jasmonic acid synthesis (Feys et al 1994;Ishiguro et al 2001;McConn and Browse 1996;Park et al 2002;Sanders et al 2000;Stintzi and Browse 2000;von Malek et al 2002). Atanassova (1999) observed up to 26% self-pollination in the most extreme cases, on cultivar "Vrbicanske nizke" (ps-2/ps-2) under Weld conditions.…”

The novel elicitor AsES triggers a defense response against Botrytis cinerea in Arabidopsis thaliana

“…Plants were grown during 4 weeks in a 12 h light/12 h dark cycle with 60-70% of relative humidity, with a day temperature of 20-22 • C and a night temperature of 16-18 • C. A. thaliana ecotype Columbia-0 (Col-0) wild-type plants were obtained from the Nottingham Arabidopsis Stock Centre (Nottingham, UK), transgenic seeds over-expressing the salicylate hydroxylase NahG gene were obtained from J. Ryals [23]. The following A. thaliana mutants (all in the Col-0 background) were used and previously described: jar1-1, coi1-16, etr1-1, ein2-1 [24], ics1 [25], npr1 [26], and dde2.1 [27].…”

Functional conservation and maintenance of expression pattern of FIDDLEHEAD-like genes in Arabidopsis and Antirrhinum

“…Several dehiscence mutants are available in Arabidopsis (Sanders et al, 1999) that could be helpful in establishing the role of the FDH gene in the process of cell separation within the stomium. Like FDH, the anther dehiscence genes that have so far been identified molecularly, DEFECTIVE IN ANTHER DEHISCENCE 1 (DAD1) (Ishiguro et al, 2001), DELAYED DEHISCENCE 1 (Sanders et al, 2000) and OPR3 (Stintzi and Browse, 2000), all encode enzymes of lipid metabolism.…”