Flower development in carrot CMS plants: mitochondria affect the expression of MADS box genes homologous to GLOBOSA and DEFICIENS


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Maternally inherited defects in the formation of male flower organs leading to cytoplasmic male sterility (CMS) indicate an involvement of mitochondrial genes in the control of flower formation. In the ‘carpeloid’ CMS type of carrot, stamens are replaced by carpels. The florets thus resemble well-investigated homeotic flower mutants of Arabidopsis and Antirrhinum, in which organ identity is impaired because of the mutation of specific nuclear MADS box genes. We have isolated five cDNAs encoding MADS box proteins (DcMADS1–5) from a flower-specific library of carrot. Structural features deduced from their sequence and transcript patterns in unmodified carrot flowers determined by in situ hybridisation relate them to known MADS box transcription factors involved in specification of flower organs. In ‘carpeloid’ CMS flowers, we detected a distinctly reduced expression of DcMADS2 and DcMADS3, homologues of the Antirrhinum genes GLOBOSA and DEFICIENS. Our data strongly suggest that the ‘carpeloid’ CMS phenotype is caused by a cytoplasmic (mitochondrial) effect on the expression of two MADS box factors specifying organ development at whorls 2 and 3 of carrot flowers.