U.S. Department of Agriculture, Agricultural Research Service, Urbana, IL, 61801, USA; Department of Plant Biology, University of Illinois, Urbana-Champaign, IL, 61801, USA.
Department of Biological Sciences, University of Illinois at Chicago, Chicago, IL, 60607, USA.
J Plant Physiol. 2019 Oct;241:153031. doi: 10.1016/j.jplph.2019.153031. Epub 2019 Aug 23.
Seed dormancy is a critical mechanism that delays germination until environmental conditions are favorable for growth. Plant hormones gibberellin (GA) and abscisic acid (ABA) have long been recognized as key players in regulating dormancy and germination. Recent data have increased interest in brassinosteroid (BR) hormones that promote germination by activating GA downstream genes and inactivating ABA signaling. Exposure of imbibed seeds to low temperature (cold stratification) is widely used to release seed dormancy and to improve germination frequency. However, the mechanism by which cold stratification overcomes the inhibitory role of ABA is not completely understood. In the present study, we show delayed germination of seeds of the BR insensitive mutant, bri1-5, that was largely reversed by treatment with fluridone, an inhibitor of ABA biosynthesis. In addition, the bri1-5 seeds were markedly less sensitive to the cold stratification release of dormancy. These results suggest that BR locates upstream of ABA signaling and downstream of cold stratification signaling in dormancy and germination pathways. Consistent with this notion, BR biosynthetic genes, DWF4 and DET2, were upregulated by cold stratification. The transcripts of the GA biosynthesis gene, GA3ox1, and cold responsive genes, CBF1 and CBF2, increased in response to cold stratification in wild type seeds but not in bri1-5 seeds. Conversely, transgenic seeds overexpressing BRI1 germinated more rapidly than wild type in the absence of cold stratification. Thus, we propose that BR signaling plays a previously unrecognized role in the cold stratification pathway for seed dormancy and germination.
种子休眠是一种关键机制，它延迟了种子的萌发，直到环境条件有利于生长。植物激素赤霉素（GA）和脱落酸（ABA）长期以来一直被认为是调节休眠和萌发的关键因素。最近的数据增加了对油菜素内酯（BR）激素的兴趣，BR 激素通过激活 GA 下游基因和失活 ABA 信号来促进萌发。将吸胀的种子暴露于低温（低温层积）中被广泛用于解除种子休眠并提高萌发频率。然而，低温层积克服 ABA 抑制作用的机制尚不完全清楚。在本研究中，我们显示 BR 不敏感突变体 bri1-5 的种子发芽延迟，该延迟主要通过 ABA 生物合成抑制剂 fluridone 处理得到逆转。此外，bri1-5 种子对低温层积解除休眠的敏感性明显降低。这些结果表明，BR 在休眠和萌发途径中位于 ABA 信号的上游和低温层积信号的下游。这一观点与 BR 生物合成基因 DWF4 和 DET2 被低温层积上调的结果一致。GA 生物合成基因 GA3ox1 和冷响应基因 CBF1 和 CBF2 的转录物在野生型种子中响应低温层积而增加，但在 bri1-5 种子中则没有。相反，过表达 BRI1 的转基因种子在没有低温层积的情况下比野生型种子更快地发芽。因此，我们提出 BR 信号在种子休眠和萌发的低温层积途径中发挥了以前未被认识到的作用。
