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Multiple roles of the transcription factor AtMYBR1/AtMYB44 in ABA signaling, stress responses, and leaf senescence.

Jaradat MR, Feurtado JA, Huang D, Lu Y, Cutler AJ - BMC Plant Biol. (2013)

Bottom Line: 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.MYBR1 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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Plant Biotechnology Institute, National Research Council of Canada, 110 Gymnasium Place, Saskatoon S7N 0W9, Canada. adrian.cutler@nrc-cnrc.gc.ca.

ABSTRACT

Background: The 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.

Results: When 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.

Conclusions: MYBR1 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.

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Expression pattern of 24 stress responsive genes in WT and gain- and loss of AtMYBR1 function mutant genotypes with and without PBI425. Comparisons are relative to (i) WT without PBI425 treatment for columns 1, 2 and 4 and (ii) WT with PBI425 treatment for columns 3 and 5 from left to right.
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Figure 2: Expression pattern of 24 stress responsive genes in WT and gain- and loss of AtMYBR1 function mutant genotypes with and without PBI425. Comparisons are relative to (i) WT without PBI425 treatment for columns 1, 2 and 4 and (ii) WT with PBI425 treatment for columns 3 and 5 from left to right.

Mentions: Many stress genes that are highly induced by ABA, are repressed by MYBR1 (Figure 2). However, since MYBR1 did not appear to repress all PBI425 induced genes, we examined more closely the gene expression patterns affected by MYBR1 and PBI425. In this analysis, we added 32 statistically significant genes to the total gene list of Table 1 for detailed analysis and interpretation. These 32 genes were not listed in Table 1 since their fold change was below the 1.5 ratio threshold. However, changes in expression of these genes were either verified by qPCR and direct spot visualization in BASE or were present in our comparative analysis of our microarray data with data published by van der Graaff et al. [22].


Multiple roles of the transcription factor AtMYBR1/AtMYB44 in ABA signaling, stress responses, and leaf senescence.

Jaradat MR, Feurtado JA, Huang D, Lu Y, Cutler AJ - BMC Plant Biol. (2013)

Expression pattern of 24 stress responsive genes in WT and gain- and loss of AtMYBR1 function mutant genotypes with and without PBI425. Comparisons are relative to (i) WT without PBI425 treatment for columns 1, 2 and 4 and (ii) WT with PBI425 treatment for columns 3 and 5 from left to right.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4219380&req=5

Figure 2: Expression pattern of 24 stress responsive genes in WT and gain- and loss of AtMYBR1 function mutant genotypes with and without PBI425. Comparisons are relative to (i) WT without PBI425 treatment for columns 1, 2 and 4 and (ii) WT with PBI425 treatment for columns 3 and 5 from left to right.
Mentions: Many stress genes that are highly induced by ABA, are repressed by MYBR1 (Figure 2). However, since MYBR1 did not appear to repress all PBI425 induced genes, we examined more closely the gene expression patterns affected by MYBR1 and PBI425. In this analysis, we added 32 statistically significant genes to the total gene list of Table 1 for detailed analysis and interpretation. These 32 genes were not listed in Table 1 since their fold change was below the 1.5 ratio threshold. However, changes in expression of these genes were either verified by qPCR and direct spot visualization in BASE or were present in our comparative analysis of our microarray data with data published by van der Graaff et al. [22].

Bottom Line: 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.MYBR1 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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Plant Biotechnology Institute, National Research Council of Canada, 110 Gymnasium Place, Saskatoon S7N 0W9, Canada. adrian.cutler@nrc-cnrc.gc.ca.

ABSTRACT

Background: The 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.

Results: When 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.

Conclusions: MYBR1 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.

Show MeSH
Related in: MedlinePlus