Overexpression of Arabidopsis ESR1 induces initiation of shoot regeneration
Overexpression of Arabidopsis ESR1 induces initiation of shoot regeneration
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DOI：
10.1105/tpc.13.12.2609
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发表时间：
2001-12-01
期刊：
影响因子：
11.6
通讯作者：
Chua, NH
中科院分区：
文献类型：
--
作者：
Banno, H;Ikeda, Y;Chua, NH
拟南芥cDNA文库的功能筛选能够鉴定一种新的cDNA，ESR 1（用于芽再生增强剂），当在拟南芥根外植体中过表达时，它可以赋予细胞分裂素独立的芽形成。无论是愈伤组织的诱导，也没有根的形成受到影响ESR 1过表达。ESR 1编码一个具有AP 2/EREBP结构域的转录因子。令人惊讶的是，ESR 1过表达也大大提高了在细胞分裂素存在下从根外植体再生芽的效率，该过程所需的最佳细胞分裂素浓度发生了变化。ESR 1过表达对芽再生的影响与细胞分裂素的影响是协同的。过量表达ESR 1不能诱导愈伤组织形成或根形成，这表明其作用是特异性的芽形成。在野生型拟南芥中，细胞分裂素诱导ESR 1的表达。ESR 1的转录水平也增加了短暂的芽再生过程中从根外植体，最有可能在芽诱导培养基中的细胞分裂素。这种短暂的增加发生在获得再生能力之后和芽形成之前，这与ESR 1过表达的生理效应一致。我们的研究结果表明，ESR 1可以调节芽再生的诱导后，收购的器官发生的能力。
Functional screening of an Arabidopsis cDNA library enabled the identification of a novel cDNA, ESR1 (for Enhancer of Shoot Regeneration), that can confer cytokinin-independent shoot formation when overexpressed in Arabidopsis root explants. Neither callus induction nor root formation was affected by ESR1 overexpression. ESR1 encodes a putative transcription factor with an AP2/EREBP domain. Surprisingly, ESR1 overexpression also greatly increased the efficiency of shoot regeneration from root explants in the presence of cytokinin, with a shift in the optimal cytokinin concentration required for this process. The effects of ESR1 overexpression on shoot regeneration are synergistic with those of cytokinin. Overexpression of ESR1 cannot induce callus formation or root formation, suggesting that its effects are specific to shoot formation. In wild-type Arabidopsis plants, ESR1 expression was induced by cytokinin. ESR1 transcript levels also increased transiently during shoot regeneration from root explants, most probably in response to cytokinin in the shoot-inducing medium. This transient increase occurred after the acquisition of competence for regeneration and before shoot formation, which is consistent with the physiological effects of ESR1 overexpression. Our results suggest that ESR1 may regulate the induction of shoot regeneration after the acquisition of competence for organogenesis.