The brassinosteroid receptor kinase, BRI1, plays a role in seed germination and the release of dormancy by cold stratification.

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.