ABSTRACT
Gibberellic acid (GA) plays a key role in seed germination through coordinate interactions with other growth hormones and external signals. However, the way in which external signals are incorporated into the GA-signaling pathway is largely unknown. Here, we demonstrate that a membrane-bound NAC transcription factor NTL8 mediates the salt regulation of seed germination via the GA pathway, primarily independently of ABA. NTL8 is induced by high salinity. Its expression is also elevated by a GA biosynthetic inhibitor paclabutrazol (PAC), but is repressed by GA. Notably, high salinity greatly represses the GA3 oxidase 1 (GA3ox1) gene, supporting the hypothesis that salt signals inhibit seed germination by repressing GA biosynthesis. Induction of NTL8 and repression of GA3ox1 by high salinity still occur in the ABA-deficient aba3-1 mutant. Accordingly, the germination of a T-DNA insertional ntl8-1 mutant seed is resistant to high salinity and PAC. Interestingly, NTL8 is significantly induced during cold imbibition, but the induction declines quickly in germinating seeds, like RGL2. NTL8 activity is also regulated by controlled proteolytic release of the membrane-bound NTL8 form. Its release from the membranes is activated by PAC and high salinity. Our data support that NTL8 modulates GA-mediated salt signaling in regulating seed germination. This regulatory scheme may provide an adaptative fitness, which delays seed germination under high salinity conditions.
Subject(s)
Arabidopsis Proteins/metabolism , Arabidopsis/metabolism , Germination , Gibberellins/biosynthesis , Salinity , Signal Transduction , Abscisic Acid/metabolism , Arabidopsis/growth & development , Cold Temperature , Gibberellins/antagonists & inhibitors , Seeds/growth & development , Seeds/metabolism , Transcription Factors/metabolism , Triazoles/pharmacologyABSTRACT
Pathogenesis-related (PR) proteins are a group of heterogeneous proteins encoded by genes that are rapidly induced by pathogenic infections and by salicylic acid (SA), jasmonic acid (JA) and ethylene (ET). They are widely used as molecular markers for resistance response to pathogens and systemic acquired response (SAR). However, recent studies have shown that the PR genes are also regulated by environmental factors, including light and abiotic stresses, and by developmental cues, suggesting that they also play a role in certain stress responses and developmental processes. In this work, we systematically examined the expression patterns of Arabidopsis PR genes. We also investigated the effects of environmental stresses and growth hormones on the expression of PR genes. We found that individual PR genes are temporally and spatially regulated in distinct patterns. In addition, they are differentially regulated by plant growth hormones, including SA, ABA, JA, ET and brassinosteroid (BR), and by diverse abiotic stresses, supporting the contention that the PR proteins play a role in plant developmental processes other than disease resistance response. Interestingly, PR-3 was induced significantly by high salt in an ABA-dependent manner. Consistent with this, a T-DNA insertional knockout plant with disruption of the PR-3 gene showed a significantly reduced rate of seed germination in the presence of high salt. It is thus proposed that PR-3 mediates ABA-dependent salt stress signals that affect seed germination in Arabidopsis. PR-4 and PR-5 also contributed to salt regulation of seed germination, although their effects were not as evident as those of PR-3.
Subject(s)
Arabidopsis Proteins/metabolism , Arabidopsis/genetics , Arabidopsis/metabolism , Gene Expression Profiling , Germination/drug effects , Seeds/drug effects , Seeds/growth & development , Sodium Chloride/pharmacology , Arabidopsis Proteins/genetics , Gene Expression Regulation, Plant/drug effects , Gene Expression Regulation, Plant/physiology , Genes, Plant/geneticsABSTRACT
An Arabidopsis GH3 gene WES1 encodes an auxin-conjugating enzyme that plays a role in stress responses by modulating endogenous levels of active auxin through a negative feedback regulation. Here, we report a photomorphogenic role for WES1 in hypocotyl growth. Hypocotyls of the WES1-overexpressing wes1-D and the knockout wes1 mutants were similar to control hypocotyls in darkness. However, the wes1-D hypocotyls were significantly shorter but the wes1 hypocotyls were longer than control hypocotyls under red light. Accordingly, WES1 transcription was up-regulated in a phytochrome B mutant. These results provide support for WES1 regulating hypocotyl growth by mediating phytochrome B-perceived light signals.
