摘要Photomorphogenesis is controlled by multiple signaling pathways,including the light and brassinosteroid (BR) pathways.BR signaling activates the BZR1 transcription factor,which is required for suppressing photomorphogenesis in the dark.We identified a suppressor of the BR hypersensitive mutant bzr1-1D and named it bzr1-1D suppressor1-Dominant (bzs1-D).The bzs1-D mutation was caused by overexpression of a B-box zinc finger protein BZS1,which is transcriptionally repressed by BZR1.Overexpression of BZS1 causes de-etiolation in the dark,short hypocotyls in the light,reduced sensitivity to BR treatment,and repression of many BR-activated genes.Knockdown of BZS1 by co-suppression partly suppressed the short hypocotyl phenotypes of BR-deficient or insensitive mutants.These results support that BZS1 is a negative regulator of BR response.BZS1 overexpressors are hypersensitive to different wavelengths of light and loss of function of BZS1 reduces plant sensitivity to light and partly suppresses the constitutive photomorphogenesis 1 (cop1) mutant in the dark,suggesting a positive role in light response.BZS1 protein accumulates at an increased level after light treatment of dark-grown BZS1-OX plants and in the cop1 mutants,and BZS1 interacts with COP1 in vitro,suggesting that light regulates BZS1 through COP1-mediated ubiquitination and proteasomal degradation.These results demonstrate that BZS1 mediates the crosstalk between BR and light pathways.