PIF4 negatively modulates cold tolerance in tomato anthers via temperature-dependent regulation of tapetal cell death
PIF4 negatively modulates cold tolerance in tomato anthers via temperature-dependent regulation of tapetal cell death
复制标题
PIF4 通过温度依赖性调节绒毡层细胞死亡来负向调节番茄花药的耐冷性。
DOI：
10.1093/plcell/koab120
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发表时间：
2021-05-02
期刊：
影响因子：
11.6
通讯作者：
Lu, Gang
中科院分区：
文献类型：
--
作者：
Pan, Changtian;Yang, Dandan;Lu, Gang
极端温度条件严重影响植物雄性生殖发育；然而，花药对极端温度反应的分子机制仍然没有得到很好的描述。转录因子光敏色素相互作用因子4 （phytochrome-interacting factor4, PIF4）是整合多种信号通路的中枢，调控植物的热感觉生长和结构适应。在此，我们报道了番茄（Solanum lycopersicum）中SIPIF4在调控花药耐寒性中起关键作用。CRISPR（聚集规律间隔短回传重复序列）相关核酸酶cas9产生的SIPIF4敲除突变体由于绒毡层温度敏感性降低，在花粉中表现出增强的耐寒性，而过表达SIPIF4通过延迟绒毡层程序性细胞死亡（PCD）而使花粉败育。SIPIF4直接与SIDYT1相互作用，SIDYT1是SITDF1的直接上游调控因子，两者（SIDYT1和SITDF1）在绒毡层发育和绒毡层PCD的调控中发挥重要作用。中低温（MLT）通过SIPIF4- sidyt1复合物促进SITDF1的转录激活，导致花粉败育，而敲除SIPIF4则阻断了MLT诱导的SITDF1的激活。此外，SIPIF4直接与SIDYT1启动子中的规范E-box序列结合。总之，这些发现表明，SIPIF4通过直接与绒毡层调控模块以温度依赖的方式负向调控花药的耐寒性。我们的研究结果揭示了花药适应低温的分子机制。
Extreme temperature conditions seriously impair male reproductive development in plants; however, the molecular mechanisms underlying the response of anthers to extreme temperatures remain poorly described. The transcription factor phytochrome-interacting factor4 (PIF4) acts as a hub that integrates multiple signaling pathways to regulate thermosensory growth and architectural adaptation in plants. Here, we report that SIPIF4 in tomato (Solanum lycopersicum) plays a pivotal role in regulating cold tolerance in anthers. CRISPR (clustered regularly interspaced short palindromic repeats)-associated nuclease Cas9-generated SIPIF4 knockout mutants showed enhanced cold tolerance in pollen due to reduced temperature sensitivity of the tapetum, while overexpressing SIPIF4 conferred pollen abortion by delaying tapetal programmed cell death (PCD). SIPIF4 directly interacts with SIDYT1, a direct upstream regulator of SITDF1, both of which (SIDYT1 and SITDF1) play important roles in regulating tapetum development and tapetal PCD. Moderately low temperature (MLT) promotes the transcriptional activation of SITDF1 by the SIPIF4-SIDYT1 complex, resulting in pollen abortion, while knocking out SIPIF4 blocked the MLT-induced activation of SITDF1. Furthermore, SIPIF4 directly binds to the canonical E-box sequence in the SIDYT1 promoter. Collectively, these findings suggest that SIPIF4 negatively regulates cold tolerance in anthers by directly interacting with the tapetal regulatory module in a temperature-dependent manner. Our results shed light on the molecular mechanisms underlying the adaptation of anthers to low temperatures.