Abstract
The cvp1 mutant is characterized by a discontinuous venation pattern with aberrant vascular cell morphology. This defect is first apparent in the spatial distribution of provascular cells during embryogenesis, suggesting that CVP1 acts early in vein patterning. We have positionally cloned the CVP1 gene and found that it encodes C-24 sterol methyltransferase 2 (SMT2), an enzyme in the sterol biosynthetic pathway. As predicted from the role of SMT2, sterol levels were significantly altered in cvp1 alleles. In the wild type, a ratio of campesterol to sitosterol was ca. 0.2, whereas in cvp1 alleles, the ratio was 1.9 or greater. The degree in sterol levels of the alleles was proportional to the severity of their phenotypes. The cvp1 mutant had normal brassinosteroid levels, and the application of brassinosteroid did not rescue the mutant phenotype. Our results indicate a brassinosteroid-independent role for sterols in vascular patterning.
