Plant Biotechnology Institute, National Research Council of Canada, 110 Gymnasium Place, Saskatoon S7N 0W9, Canada.
BMC Plant Biol. 2013 Nov 28;13:192. doi: 10.1186/1471-2229-13-192.
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.
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.
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.
转录因子 AtMYBR1（MYB44）是 MYB 转录因子家族的成员，在植物生命周期中表达，尤其是在衰老和受伤的叶片中表达。先前已表明它参与了非生物胁迫的反应，并受磷酸化调节。
当 MYBR1 在拟南芥中受组成型 35S 启动子的控制过表达（OxMYBR1）时，叶片衰老被延迟。相比之下，功能丧失的 mybr1 植物表现出更快的叶绿素丧失和衰老。MYBR1 启动子在受伤后立即强烈驱动β-葡萄糖醛酸酶报告基因在组织中的表达，并且许多受伤/发病基因在 OxMYBR1 中下调。OxMYBR1 植物在水分胁迫下比野生型更容易受到伤害，这与 OxMYBR1 中许多 ABA 诱导的应激基因的抑制有关。相反，mybr1 植物对水分胁迫更耐受，并表现出叶片水分丧失率降低。MYBR1 与 ABA 受体 PYR1-LIKE8（PYL8）物理相互作用，表明 MYBR1 直接参与早期 ABA 信号转导。MYBR1 似乎与 AtMYBR2（MYB77）具有部分冗余功能，并且双 mybr1 X mybr2 突变体表现出比单个 mybr1 和 mybr2 突变体更强的衰老和应激相关表型。
MYBR1 是 ABA、应激、受伤反应的负调节剂，并阻止衰老。它似乎具有维持生长过程的动态平衡功能，以应对物理损伤或应激。
