The Arabidopsis embryo mutant schlepperless has a defect in the chaperonin-60α gene

We identified a T-DNA-generated mutation in the chaperonin-60 alpha gene of Arabidopsis that produces a defect in embryo development. The mutation, termed schlepperless (slp), causes retardation of embryo development before the heart stage, even though embryo morphology remains normal. Beyond the heart stage, the sip mutation results in defective embryos with highly reduced cotyledons. sip embryos exhibit a normal apical-basal pattern and radial tissue organization, but they are morphologically retarded. Even though sip embryos are competent to transcribe two late-maturation gene markers, this competence is acquired more slowly as compared with wild-type embryos, sip embryos also exhibit a defect in plastid development-they remain white during maturation in planta and in culture. Hence, the overall developmental phenotype of the sip mutant reflects a lesion in the chloroplast that affects embryo development. The slp phenotype highlights the importance of the chaperonin-60a protein for chloroplast development and subsequently for the proper development of the plant embryo and seedling.