The Arabidopsis Embryo Mutant schlepperless Has a Defect in the Chaperonin-60α Gene

Abstract

We identified a T-DNA-generated mutation in the chaperonin-60␣ 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 slp mutation results in defective embryos with highly reduced cotyledons. slp embryos exhibit a normal apical-basal pattern and radial tissue organization, but they are morphologically retarded. Even though slp embryos are competent to transcribe two late-maturation gene markers, this competence is acquired more slowly as compared with wild-type embryos. slp 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 slp mutant reflects a lesion in the chloroplast that affects embryo development. The slp phenotype highlights the importance of the chaperonin-60␣ protein for chloroplast development and subsequently for the proper development of the plant embryo and seedling.

Analysis of chlorophyll fluorescence reveals stage specific patterns of chloroplast-containing cells during Arabidopsis embryogenesis

“…Although it has been reported previously that chloroplasts are present in the late stages of Arabidopsis embryogenesis (Apuya et al, 2002;Apuya et al, 2001;GutierrezNava et al, 2004) and that chlorophyll fluorescence is widely used as a background marker in embryo imaging, to our knowledge a detailed description of the embryonic stages and cell types that contain chloroplasts have not been reported previously. In order to determine if stage specific patterns of chloroplast-containing cells are present during Arabidopsis embryogenesis, we have quantified chlorophyll fluorescence as a marker for plastids that have differentiated into chloroplasts.…”

The Omp85-Related Chloroplast Outer Envelope Protein OEP80 Is Essential for Viability in Arabidopsis

“…Because no such early defects were observed in the AtOEP80 knockout, the oep80 mutant phenotype can be considered somewhat less severe and later acting than tic110. Nevertheless, the oep80-mediated block in growth occurs considerably earlier than the stage during which photosynthetic establishment normally commences (heart stage; Apuya et al, 2001), and so the data indicate that the role of AtOEP80 is not directly associated with photosynthesis.…”

“…There are numerous precedents for embryo lethality caused by lesions in chloroplast proteins (Uwer et al, 1998;Apuya et al, 2001). In fact, in a large-scale screen for mutations affecting seed development, .25% of the identified loci were predicted to encode plastidic proteins (McElver et al, 2001).…”

Altered expression of the Arabidopsis ortholog of DCL affects normal plant development

“…This defect in chloroplast biogenesis that affects plant organ development is similar to that observed in many chloroplast developmental mutants. For instance, null mutations of the nuclear-encoded chloroplast genes EDD1, SLP, Emb506 and DCL cause embryo abortion (Uwer et al 1998;Albert et al 1999;Apuya et al 2001;Despres et al 2001;Bellaoui et al 2003). Similarly, mutations that block chloroplast biogenesis and alter palisade cell morphogenesis have been identified, and suggest that chloroplast development also regulates leaf differentiation (Reiter et al 1994;Chatterjee et al 1996;Babiychuk et al 1997;Keddie et al 1996;Wang et al 2000).…”