MdMYB46 could enhance salt and osmotic stress tolerance in apple by directly activating stress-responsive signals
MdMYB46 could enhance salt and osmotic stress tolerance in apple by directly activating stress-responsive signals
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DOI：
10.1111/pbi.13151
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发表时间：
2019-12-01
影响因子：
13.8
通讯作者：
Zhang, Zhihong
中科院分区：
文献类型：
--
作者：
Chen, Keqin;Song, Mengru;Zhang, Zhihong
为扩大苹果（Malusxanditica Borkh.）并通过基因工程手段选育抗盐品种，有必要阐明苹果耐盐和耐渗透胁迫的机理。对MdMYB 46转录因子进行了鉴定，并对MdMYB 46过表达和MdMYB 46-RNAi苹果株系进行了胁迫处理试验，结果表明MdMYB 46能够提高苹果耐盐性和耐渗透胁迫性。在转基因拟南芥和苹果中，MdMYB 46通过直接与木质素生物合成相关基因的启动子结合，促进次生细胞壁的生物合成和木质素的沉积。为了探讨MdMYB 46是否能够协调胁迫信号转导途径，协同次生壁的形成，增强植物的抗逆性，筛选出与渗透胁迫、盐胁迫以及MdMYB 46转录水平正相关的MdABRE 1A、MdDREB 2A和脱水响应基因MdRD 22、MdRD 29 A。进一步的验证试验表明，MdMYB 46可以通过直接结合这些基因的启动子来激活它们的转录。上述结果表明，MdMYB 46不仅通过激活次生细胞壁生物合成途径，而且还通过直接激活胁迫响应信号，增强苹果对盐和渗透胁迫的耐受性。
To expand the cultivation area of apple (Malusxdomestica Borkh.) and select resistant varieties by genetic engineering, it is necessary to clarify the mechanism of salt and osmotic stress tolerance in apple. The MdMYB46 transcription factor was identified, and the stress treatment test of MdMYB46-overexpressing and MdMYB46-RNAi apple lines indicated that MdMYB46 could enhance the salt and osmotic stress tolerance in apple. In transgenic Arabidopsis and apple, MdMYB46 promoted the biosynthesis of secondary cell wall and deposition of lignin by directly binding to the promoter of lignin biosynthesis-related genes. To explore whether MdMYB46 could coordinate stress signal transduction pathways to cooperate with the formation of secondary walls to enhance the stress tolerance of plants, MdABRE1A, MdDREB2A and dehydration-responsive genes MdRD22 and MdRD29A were screened out for their positive correlation with osmotic stress, salt stress and the transcriptional level of MdMYB46. The further verification test demonstrated that MdMYB46 could activate their transcription by directly binding to the promoters of these genes. The above results indicate that MdMYB46 could enhance the salt and osmotic stress tolerance in apple not only by activating secondary cell wall biosynthesis pathways, but also by directly activating stress-responsive signals.