FAR-RED INSENSITIVE 219/JAR1與phytochrome B透過調控核斑型態共同抑制阿拉伯芥之遮蔭反應

Abstract

遮蔭環境所促使的植物生長通常伴隨著抑制植物對於病蟲害抵禦的能力。根據現有研究可知phytochrome B (phyB) 可以透過調控茉莉酸(JAs)生合成及訊息傳遞路徑中的多個關鍵分子來抑制植物的防禦反應，如JAZs，MYCs，ST2a等。因此本研究想探討活化態茉莉酸(JA-Ile)關鍵之合成酵素FAR-RED INSENSITIVE 219 (FIN219)是否也參與在phyB所調控的生長與防禦之權衡反應中。研究中指出FIN219在避蔭反應之中扮演負調控者，同時也與phyB有直接的交互作用。有趣的是從實驗結果中發現活化態的FIN219在遮蔭環境中為主要的表現型態，然而，此現象與已知遮蔭環境下防禦反應會被削弱的論點有所衝突。因此這也暗示在遮蔭環境下phyB與FIN219的結合可能有特別的調控關係，推測phyB會透過與FIN219的直接結合去削弱其調控之茉莉酸訊息傳遞反應。此外本研究也發現外源性茉莉酸(MeJA)處理以及內源性大量表現茉莉酸的突變株dgd1-1皆可透過促使細胞核中phyB核斑(nuclear speckles)的形成，直接抑制植物遮蔭反應中的下胚軸生長。從轉錄體分析的結果中也可以發現phyB與FIN219以協同方式抑制避蔭反應相關基因的表現，如HFR1，IAA29等。藉此得知phyB所調控的避蔭反應中有部分路徑需要FIN219參與，同時也有部分路徑是獨立於FIN219調控之外。綜合以上資訊，本研究提出一個避蔭反應調控機制的模型：在植物受到遮蔭的情況下，細胞質中的phyB會透過與活化態的FIN219結合，干擾茉莉酸的訊息傳遞反應，並且導致細胞核中的phyB核斑瓦解，因此植物得以促使一系列避蔭反應相關基因的表現，向上生長延長以獲得足夠的光照能量，最終適應遮蔭的環境。

Shade-triggered plant growth is regularly associated with attenuating the capability of plants’ innate immune responses against herbivores. According to previous reports, phytochrome B (phyB) repressed defense response under the shaded environment by regulating several critical components in JA signaling pathway, such as JAZs, MYCs, and ST2a. However, whether the JA-Ile biosynthetic enzyme FAR-RED INSENSITIVE 219 (FIN219), is involved in the phyB-mediated growth-defense tradeoff has not been reported. Our studies showed that FIN219 played a negative role in shade avoidance response and showed physical interaction with phyB under shading conditions. Interestingly, the active form of FIN219 is present under shading conditions by analyzing the phosphorylation state of FIN219. Combined with the up-regulated expression level of JA-responsive genes in phyB-deficient mutants under shade, it implies that phyB might suppress the JA response by directly targeting FIN219. On the other hand, we found that exogenous JA treatment and the high level of endogenous JA in the dgd1-1 mutant promote the formation of nuclear speckles of phyB even in the shaded environment, leading to the photomorphogenic phenotype. Moreover, the microarray analysis showed that phyB and FIN219 co-suppressed the expression of typical SAR marker genes, HFR1 and IAA29. Our data suggest that phyB negatively regulates SAR via FIN219-dependent and FIN219-independent pathways. Taken together, phyB represses the signaling transduction of JA via physically interacting with FIN219, resulting in the deconstruction of phyB-associated nuclear speckles so that the plants can elongate rapidly for sufficient light absorption under shade environments.