2016年7月11日，學術刊物自然出版集團旗下子刊《Nature Communications》雜志在線發表了*植物研究所張立新研究員發表的一篇研究論文，研究發現質體與細胞核的交流涉及了鈣調節的MAPK信號通路。
質體是植物細胞*的細胞器，可以分為葉綠體、有色體和白色體。葉綠體(chloroplast)含有葉綠素，是植物進行光合作用的重要場所。葉綠體的功能特性受到細胞核基因組的嚴密調控。而葉綠體逆向信號可調控質體和細胞核基因的表達，幫助植物應對外界環境的改變，正確生產葉綠體并維持其功能。不過，人們對葉綠體的逆向信號傳導還知之甚少。
細胞核能夠感知葉綠體壓力并做出相應的反應，誘導或抑制編碼質體蛋白的細胞核基因。此前的研究顯示，ABI4在葉綠體逆向信號通路中抑制LHCB基因。現在研究人員揭示了逆向信號通路的另一個調控機制。他們發現，MAP激酶MPK3/MPK6磷酸化并激活ABI4。而MAPK的活化涉及葉綠體鈣結合蛋白CAS介導的鈣瞬變。研究表明，葉綠體調節的Ca2+信號會控制MAPK通路，激活葉綠體逆向信號鏈中的關鍵組分。
原文摘要：
Chloroplast retrograde signals play important roles in coordinating the plastid and nuclear gene expression and are critical for proper chloroplast biogenesis and for maintaining optimal chloroplast functions in response to environmental changes in plants. Until now, the signals and the mechanisms for retrograde signalling remain poorly understood. Here we identify factors that allow the nucleus to perceive stress conditions in the chloroplast and to respond accordingly by inducing or repressing specific nuclear genes encoding plastid proteins. We show that ABI4, which is known to repress the LHCB genes during retrograde signalling, is activated through phosphorylation by the MAP kinases MPK3/MPK6 and the activity of these kinases is regulated through 14-3-3ω-mediated Ca2+-dependent scaffolding depending on the chloroplast calcium sensor protein CAS. These findings uncover an additional mechanism in which chloroplast-modulated Ca2+ signalling controls the MAPK pathway for the activation of critical components of the retrograde signalling chain.
