鹽脅迫是最典型的非生物脅迫之一，嚴重影響植物的生長發育及農作物的產量。植物在長期的進化過程獲得了高度完整的感知和響應鹽脅迫的信號轉導途徑來協調植物的脅迫耐受及生長發育過程。目前我們對於植物如何感受土壤中鹽濃度，進而通過調節生長發育過程以適應鹽脅迫環境的分子機制還缺乏認識。
中國科學院遺傳與發育生物學研究所鮑時來研究組以模式植物擬南芥為材料，利用遺傳學和生物化學等研究手段，揭示了蛋白質精氨酸甲基轉移酶SKB1在植物耐受鹽脅迫和生長發育過程中起重要作用。該研究發現SKB1的功能缺失導致擬南芥對鹽脅迫的超敏感、生長遲緩及晚花等缺陷。SKB1的突變導致了植物喪失協調鹽脅迫耐受和生長發育（比如開花時間）的能力，使植物一直處於脅迫響應狀態而限制了植物的生長過程。在正常生長條件下，SKB1結合於RD29A、RD29B等脅迫響應基因及開花抑制基因FLC的染色質區並催化這些區域的組蛋白H4R3的對稱性雙甲基花，抑制這些基因的表達，以促進開花等發育過程；在受到鹽脅迫時，SKB1從這些基因的染色質區離開，增加SKB1介導的mRNA剪接複合體中心蛋白LSM4的對稱性雙甲基化，從而使脅迫響應基因及開花抑制基因被誘導表達，同時增強了非生物脅迫響應基因及開花等生長發育相關基因的剪接。因此，植物通過改變SKB1介導的組蛋白H4R3的對稱性雙甲基化(H4R3sme2)和mRNA剪接複合體中心蛋白LSM4的對稱性雙甲基化來協調鹽脅迫耐受及生長發育過程。
該研究發現了蛋白質精氨酸甲基化轉移酶SKB1是植物感知脅迫並協調發育過程的重要因子，深化了我們對植物適應環境的機制的認識。鮑時來實驗室博士研究生張照亮為該文第一作者。該項目得到了國家自然科學基金項目、重大研究計劃和973項目的資助。（生物谷Bioon.com）
生物谷推薦原文出處：
Plant Cell doi:10.1105/tpc.110.081356
Arabidopsis Floral Initiator SKB1 Confers High Salt Tolerance by Regulating Transcription and Pre-mRNA Splicing through Altering Histone H4R3 and Small Nuclear Ribonucleoprotein LSM4 Methylation[C],[W]
Zhaoliang Zhanga,b,1, Shupei Zhanga,1, Ya Zhanga, Xin Wanga, Dan Lia, Qiuling Lia,b, Minghui Yuea,b, Qun Lia, Yu-e Zhanga, Yunyuan Xuc, Yongbiao Xuea,d, Kang Chongc,d and Shilai Baoa,2
a Key Laboratory of Molecular and Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China
b Graduate University of the Chinese Academy of Sciences, Beijing 100039, China
c Key Laboratory of Photosynthesis and Environmental Molecular Physiology, Institute of Botany, Chinese Academy of Sciences, Beijing 100093, China
d National Plant Gene Research Centre, Beijing 100101, China
Plants adapt their growth and development in response to perceived salt stress. Although DELLA-dependent growth restraint is thought to be an integration of the plant’s response to salt stress, little is known about how histone modification confers salt stress and, in turn, affects development. Here, we report that floral initiator Shk1 kinase binding protein1 (SKB1) and histone4 arginine3 (H4R3) symmetric dimethylation (H4R3sme2) integrate responses to plant developmental progress and salt stress. Mutation of SKB1 results in salt hypersensitivity, late flowering, and growth retardation. SKB1 associates with chromatin and thereby increases the H4R3sme2 level to suppress the transcription of FLOWERING LOCUS C (FLC) and a number of stress-responsive genes. During salt stress, the H4R3sme2 level is reduced, as a consequence of SKB1 disassociating from chromatin to induce the expression of FLC and the stress-responsive genes but increasing the methylation of small nuclear ribonucleoprotein Sm-like4 (LSM4). Splicing defects are observed in the skb1 and lsm4 mutants, which are sensitive to salt. We propose that SKB1 mediates plant development and the salt response by altering the methylation status of H4R3sme2 and LSM4 and linking transcription to pre-mRNA splicing.