Main conclusion: Jasmonic acid (JA) negatively regulates stomatal development by promoting LCD expression and hydrogen sulfide (H 2 S) biosynthesis. H 2 S inhibits the initiation of stomata formation and acts upstream of SPEECHLESS. Abstract: Stomatal development is strictly regulated by endogenous signals and environmental cues. We recently revealed that jasmonic acid (JA) negatively regulates stomatal development in Arabidopsis thaliana cotyledons (Han et al., Plant Physiol 176:2871–2885, 2018), but the underlying molecular mechanism remains largely unknown. Here, we uncovered a role for H 2 S in regulating stomatal development. The H 2 S scavenger hypotaurine reversed the JA-induced repression of stomatal development in the epidermis of wild-type Arabidopsis. The H 2 S-deficient mutant lcd displayed increased stomatal density and stomatal index values, which were rescued by treatment with sodium hydrosulfide (NaHS; an H 2 S donor) but not JA, suggesting that JA-mediated repression of stomatal development is dependent on H 2 S biosynthesis. The high stomatal density of JA-deficient mutants was rescued by exogenous NaHS treatment. Further analysis indicated that JA positively regulates LCD expression, l -cysteine desulfhydrases ( l -CDes) activity, and endogenous H 2 S content. Furthermore, H 2 S represses the expression of stomate-associated genes and functions downstream of stomate-related signaling pathway components TOO MANY MOUTHS (TMM) and STOMATAL DENSITY AND DISTRIBUTION1 (SDD1) and upstream of SPEECHLESS (SPCH). Therefore, H 2 S acts downstream of JA signaling to regulate stomatal development in Arabidopsis cotyledons.

中文翻译：

---

硫化氢作用于茉莉酸下游抑制拟南芥气孔发育

主要结论：茉莉酸 (JA) 通过促进 LCD 表达和硫化氢 (H 2 S) 生物合成负向调节气孔发育。H 2 S 抑制气孔形成的开始并作用于 SPEECHLESS 的上游。摘要：气孔发育受到内源性信号和环境因素的严格调控。我们最近发现茉莉酸 (JA) 负向调节拟南芥子叶的气孔发育（Han 等人，Plant Physiol 176:2871–2885, 2018），但其潜在的分子机制仍然未知。在这里，我们发现了 H 2 S 在调节气孔发育中的作用。H 2 S 清除剂亚牛磺酸逆转了野生型拟南芥表皮中 JA 诱导的气孔发育抑制。H 2 S 缺陷突变体 lcd 显示出增加的气孔密度和气孔指数值，这可以通过用硫氢化钠（NaHS；H 2 S 供体）而不是 JA 处理来挽救，这表明 JA 介导的气孔发育抑制依赖于H 2 S 生物合成。JA 缺陷突变体的高气孔密度被外源 NaHS 处理挽救。进一步的分析表明，JA 正向调节 LCD 表达、l-半胱氨酸脱硫酶 (l-CDes) 活性和内源性 H 2 S 含量。此外，H 2 S 抑制气孔相关基因的表达，并抑制气孔相关信号通路组件 TOO MANY MOUTHS (TMM) 和气孔密度和分布 1 (SDD1) 以及无声 (SPCH) 上游的表达。所以，