細(xì)胞分裂素參與調(diào)控植物生長發(fā)育中幾乎所有重要過程,。細(xì)胞分裂素信號(hào)轉(zhuǎn)導(dǎo)是通過一個(gè)連續(xù)磷酸傳遞（phosphorelay）而介導(dǎo)的,。在擬南芥中，被細(xì)胞分裂素激活的受體自磷酸化后,，將磷酸基團(tuán)傳遞至磷酸轉(zhuǎn)移蛋白（AHP）,，并進(jìn)一步傳遞至下游的反應(yīng)調(diào)節(jié)子（ARR）。對(duì)細(xì)胞分裂素信號(hào)轉(zhuǎn)導(dǎo)中調(diào)節(jié)機(jī)制,，特別是對(duì)磷酸傳遞的調(diào)節(jié)機(jī)制了解很少,。
中國科學(xué)院遺傳與發(fā)育生物學(xué)研究所左建儒研究組與中國科學(xué)院動(dòng)物研究所李曉明博士的合作研究發(fā)現(xiàn)一氧化氮負(fù)調(diào)控細(xì)胞分裂素信號(hào)轉(zhuǎn)導(dǎo)。一氧化氮的一個(gè)主要生化功能是對(duì)蛋白質(zhì)特異半胱氨酸殘基的巰基進(jìn)行S-亞硝基化修飾,。S-亞硝基化修飾是一種基于氧化還原的蛋白質(zhì)翻譯后修飾機(jī)制,。與磷酸化等蛋白質(zhì)翻譯后修飾機(jī)制類似，S-亞硝基化修飾參與調(diào)控其靶蛋白的生物學(xué)活性,。左建儒研究組發(fā)現(xiàn)S-亞硝基化修飾細(xì)胞分裂素信號(hào)通路的重要組分AHP1后,，抑制AHP1及其下游組分ARR1的磷酸化，從而負(fù)調(diào)控細(xì)胞分裂素信號(hào)轉(zhuǎn)導(dǎo)以及植物對(duì)細(xì)胞分裂素的響應(yīng),。該項(xiàng)研究為解析細(xì)胞分裂素信號(hào)通路感受氧化還原信號(hào)進(jìn)而調(diào)控植物生長發(fā)育的機(jī)制提供了新線索,。
該研究結(jié)果于2月26日在線發(fā)表于《自然—通訊》（Nature Communications）。左建儒研究組的馮健博士為論文的第一作者,。該項(xiàng)研究得到了國家自然科學(xué)基金的資助,。（生物谷Bioon.com）
doi:10.1038/ncomms2541
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S-nitrosylation of phosphotransfer proteins represses cytokinin signaling
Jian Feng, Chun Wang, Qingguo Chen, Hui Chen, Bo Ren, Xiaoming Li & Jianru Zuo
Cytokinin is an essential phytohormone in plant growth and development. In Arabidopsis, cytokinin signalling is mediated by a phosphorelay that sequentially transfers phosphoryl groups from the cytokinin receptors to histidine phosphotransfer proteins (AHPs) and response regulators (ARRs). However, little is known about the regulatory mechanism of the phosphorelay. Here, we show that nitric oxide negatively regulates cytokinin signalling by inhibiting the phosphorelay activity through S-nitrosylation. S-nitrosylation of AHP1 at Cys 115 represses its phosphorylation and subsequent transfer of the phosphoryl group to ARR1. A non-nitrosylatable mutation of AHP1 renders the mutant protein insensitive to nitric oxide in repressing its phosphorylation, and partially relieves the inhibitory effect of nitric oxide on the cytokinin response. Conversely, a nitrosomimetic mutation of AHP1 causes reduced phosphorylation of AHP1 and ARR1, thereby resulting in a compromised cytokinin response. These findings illustrate a mechanism by which redox signalling and cytokinin signalling coordinate plant growth and development.
