Abstract：
S-Nitrosoglutathione plays a central role in nitric oxide (NO) homeostasis, and S-nitrosoglutathione reductase (GSNOR) regulates the cellular levels of S-nitrosoglutathione across kingdoms. Here, we investigated the role of endogenous NO in shaping shoot architecture and controlling fruit set and growth in tomato (Solanum lycopersicum). SlGSNOR silencing promoted shoot side branching and led to reduced fruit size, negatively impacting fruit yield. Greatly intensified in slgsnor knockout plants, these phenotypical changes were virtually unaffected by SlGSNOR overexpression. Silencing or knocking out of SlGSNOR intensified protein tyrosine nitration and S-nitrosation and led to aberrant auxin production and signaling in leaf primordia and fruit-setting ovaries, besides restricting the shoot basipetal polar auxin transport stream. SlGSNOR deficiency triggered extensive transcriptional reprogramming at early fruit development, reducing pericarp cell proliferation due to restrictions on auxin, gibberellin, and cytokinin production and signaling. Abnormal chloroplast development and carbon metabolism were also detected in early-developing NO-overaccumulating fruits, possibly limiting energy supply and building blocks for fruit growth. These findings provide new insights into the mechanisms by which endogenous NO fine-tunes the delicate hormonal network controlling shoot architecture, fruit set, and post-anthesis fruit development, emphasizing the relevance of NO-auxin interaction for plant development and productivity.
摘要：
S-亚硝基谷胱甘肽（GSNO）在一氧化氮（NO）稳态中起着核心作用，和GSNO还原酶（GSNOR）调节跨王国的GSNO细胞水平。这里,我们研究了内源性NO在番茄（Solanumlycopersicum）中塑造枝条结构，控制坐果和生长中的作用。SlGSNOR沉默促进枝条侧分枝并导致果实大小减小，对水果产量产生负面影响。在slgsnor敲除植物中大大加强，这些表型改变实际上不受SlGSNOR过表达的影响.SlGSNOR沉默或敲除会加剧蛋白质酪氨酸硝化和S-亚硝化，并导致叶原基和坐果卵巢中生长素的异常产生和信号传导，除了限制芽基托极性生长素运输流。SlGSNOR缺陷在早期果实发育时引发了广泛的转录重编程，由于生长素的限制而减少果皮细胞增殖，赤霉素和细胞分裂素的产生和信号传导。在早期发育的NO过度积累的果实中也检测到叶绿体发育和碳代谢异常，可能会限制能源供应和水果生长的基石。这些发现为内源性NO微调控制芽结构的微妙荷尔蒙网络的机制提供了新的见解。坐果和花后果实发育，强调NO-生长素相互作用与植物发育和生产力的相关性。
