Arabidopsis constitutive photomorphogenic mutant, bls1, displays altered brassinosteroid response and sugar sensitivity Ashverya Laxmi 1 , Laju K. Paul 1 , Janny L. Peters 2 and Jitendra P. Khurana 1, * 1 Department of Plant Molecular Biology, University of Delhi South Campus, New Delhi 110021, India; 2 Department of Experimental Botany, Plant Genetics, Radboud University of Nijmegen, Toernooiveld 1, NL- 6525 ED Nijmegen, The Netherlands Received 31 December 2003; accepted in revised form 2 September 2004 Key words: Arabidopsis, brassinosteroids, de-etiolation, light-hormone interaction, sugar signalling Abstract We have isolated an Arabidopsis mutant impaired in light- and brassinosteroid (BR) induced responses, as well as in sugar signalling. The bls1 (brassinosteroid, light and sugar1) mutant displays short hypocotyl, expanded cotyledons, and de-repression of light-regulated genes in young seedlings, and leaf differentiation and silique formation on prolonged growth in dark. In light, the bls1 mutant is dwarf and develops a short root, compact rosette, with reduced trichome number, and exhibits delayed bolting. The activity of the BR inducible TCH4 and auxin inducible SAUR promoters, fused with GUS gene, is also altered in seedlings harbouring bls1 mutant background. In addition, the bls1 mutant is hypersensitive to metabolizable sugars. The short hypocotyl phenotype in dark, short root phenotype in light and sugar hypersensitivity could be rescued with BR application. Moreover, the bls1 mutant also showed higher expression of a BR biosyn- thetic pathway gene CPD, which is known to be feedback-regulated by BR. Using a genome-wide AFLP mapping strategy, the bls1 mutant has been mapped to a 1.4 Mb region of chromosome 5. Since no other mutant with essentially a similar phenotype has been assigned to this region, we suggest that the bls1 mutant defines a novel locus involved in regulating endogenous BR levels, with possible ramifications in integrating light, hormone and sugar signalling. Introduction In recent years, our understanding of how light and phytohormone signals are integrated to reg- ulate plant growth and development has im- proved considerably through the analysis of Arabidopsis mutants defective in sensing or transducing either one or both of these signals (Khurana et al., 1998; Neff et al., 2000). An array of mutants have been described, which are altered in hormone metabolism or signal transduction and show apical hook opening even in darkness. These include auxin signal transduction mutants, axr1, axr2, axr3, shy2-1D (Leyser et al., 1993; Tian and Reed, 1999; Nagpal et al., 2000) and auxin biosynthesis mutants, rty1 and sur2 (Boer- jan et al., 1995; Delarue et al., 1998), ethylene signal transduction mutants, etr, ein, hls (Bleecker et al., 1988; Guzman and Ecker, 1990; Lehman et al., 1996), cytokinin overproducers, amp1 and hoc1 (Chaudhury et al., 1993; Catterou et al., 2002) and brassinosteroid (BR) biosynthetic mu- tants, cpd, det2 and dwf4 (Li et al., 1996; Szekeres et al., 1996; Azpiroz et al., 1998). Among these mutants, axr2, axr3, shy2-1D, amp1, hoc1, cpd, det2 and dwf4 differentiate in dark and amp1, cpd, det2, axr2, axr3 and shy2-1D also accumulate higher transcript levels of some light-regulated genes in dark. The mutant abi3 also shows partial photomorphogenesis in dark (Rohde et al., 2000). These results suggest that hook opening and dif- ferentiation in dark is a highly intricate process, Plant Molecular Biology 56: 185–201, 2004. Ó 2004 Kluwer Academic Publishers. Printed in the Netherlands. 185