BackgroundThe transcription factor AtMYBR1 (MYB44) is a member of the MYB family of transcription factors and is expressed throughout the plant life cycle and especially in senescing and wounded leaves. It has previously been shown to be involved in responses to abiotic stress and is regulated by phosphorylation.ResultsWhen MYBR1 was over-expressed under the control of the constitutive 35S promoter in Arabidopsis thaliana (OxMYBR1), leaf senescence was delayed. In contrast loss-of-function mybr1 plants showed more rapid chlorophyll loss and senescence. The MYBR1 promoter strongly drove β-GLUCURONIDASE reporter gene expression in tissues immediately after wounding and many wounding/pathogenesis genes were downregulated in OxMYBR1. OxMYBR1 plants were more susceptible to injury under water stress than wildtype, which was correlated with suppression of many ABA inducible stress genes in OxMYBR1. Conversely, mybr1 plants were more tolerant of water stress and exhibited reduced rates of water loss from leaves. MYBR1 physically interacted with ABA receptor PYR1-LIKE8 (PYL8) suggesting a direct involvement of MYBR1 in early ABA signaling. MYBR1 appears to exhibit partially redundant functions with AtMYBR2 (MYB77) and double mybr1 X mybr2 mutants exhibited stronger senescence and stress related phenotypes than single mybr1 and mybr2 mutants.ConclusionsMYBR1 is a negative regulator of ABA, stress, wounding responses and blocks senescence. It appears to have a homeostatic function to maintain growth processes in the event of physical damage or stress.

SummaryChanges in gene expression produced by the application of (+)-abscisic acid (ABA) to Arabidopsis thaliana plants were compared with changes produced by the ABA structural analogs ())-ABA, (+)-8¢-acetylene ABA and ())-2¢,3¢-dihydroacetylenic abscisyl alcohol. The maximum expression of many rapidly (+)-ABA-induced genes occurred prior to peak hormone accumulation, suggesting negative feedback regulation that may be mediated by the induction of genes encoding PP2C-type protein phosphatases. For most rapidly (+)-ABA-induced genes, expression was delayed in ABA analog treatments although analogs accumulated to higher levels than did (+)-ABA. For each analog, some genes exhibited a hypersensitive response to the analog and some genes were less sensitive to the analog than to (+)-ABA. Variations in the sensitivity of gene expression to (+)-ABA and analogs reflect the different structural requirements of two or more classes of hormone receptors. By using ABA analogs to reveal and confirm weakly (+)-ABA-regulated genes, we estimate that 14% of Arabidopsis genes are ABA-regulated in aerial tissues. Treatments with the analog (+)-8¢-acetylene ABA (PBI425) led to the identification of new ABA-regulated genes. As an example, the transcription factor MYBR1 was significantly induced by PBI425, but not by (+)-ABA, and is shown to play a role in ABA signaling by phenotypic analysis of gain-of-function and loss-of-function mutants.

Asynchronous flowering of Brassica napus (canola) leads to seeds and siliques at varying stages of maturity as harvest approaches. This range of maturation can result in premature silique dehiscence (pod shattering), resulting in yield losses, which may be worsened by environmental stresses. Therefore, a goal for canola crop improvement is to reduce shattering in order to maximize yield. We performed a comprehensive transcriptome analysis on the dehiscence zone (DZ) and valve of Arabidopsis and Brassica siliques in shatter resistant and sensitive genotypes at several developmental stages. Among known Arabidopsis dehiscence genes, we confirmed that homologs of SHP1/2, FUL, ADPG1, NST1/3 and IND were associated with shattering in B. juncea and B. napus. We noted a correlation between reduced pectin degradation genes and shatter-resistance. Tension between lignified and non-lignified cells in the silique DZ plays a major role in dehiscence. Light microscopy revealed a smaller non-lignified separation layer in relatively shatter-resistant B. juncea relative to B. napus and this corresponded to increased expression of peroxidases involved in monolignol polymerization. Sustained repression of auxin biosynthesis, transport and signaling in B. juncea relative to B. napus may cause differences in dehiscence zone structure and cell wall constituents. Tension on the dehiscence zone is a consequence of shrinkage and loss of flexibility in the valves, which is caused by senescence and desiccation. Reduced shattering was generally associated with upregulation of ABA signaling and down-regulation of ethylene and jasmonate signaling, corresponding to more pronounced stress responses and reduced senescence and photosynthesis. Overall, we identified 124 cell wall related genes and 103 transcription factors potentially involved in silique dehiscence.