The DCL gene of tomato is required for chloroplast development and palisade cell morphogenesis in leaves.

Abstract

The defective chloroplasts and leaves‐mutable (dcl‐m) mutation of tomato was identified in a Ds mutagenesis screen. This unstable mutation affects both chloroplast development and palisade cell morphogenesis in leaves. Mutant plants are clonally variegated as a result of somatic excision of Ds and have albino leaves with green sectors. Leaf midribs and stems are light green with sectors of dark green tissue but fruit and petals are wild‐type in appearance. Within dark green sectors of dcl‐m leaves, palisade cells are normal, whereas in albino areas of dcl‐m leaves, palisade cells do not expand to become their characteristic columnar shape. The development of chloroplasts from proplastids in albino areas is apparently blocked at an early stage. DCL was cloned using Ds as a tag and encodes a novel protein of approximately 25 kDa, containing a chloroplast transit peptide and an acidic alpha‐helical region. DCL protein was imported into chloroplasts in vitro and processed to a mature form. Because of the ubiquitous expression of DCL and the proplastid‐like appearance of dcl‐affected plastids, the DCL protein may regulate a basic and universal function of the plastid. The novel dcl‐m phenotype suggests that chloroplast development is required for correct palisade cell morphogenesis during leaf development.

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

“…2). This is consistent with the expression pattern of tomato DCL, which is also expressed in all types of tissues and stages of development examined (Keddie et al 1996). A 1.2-kb transcript was detected in the four organs examined, consistent with the size determined by sequencing the full-length cDNA of AtDCL.…”

“…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). Because the primary defect in all of these mutants appears to be in chloroplast development, we suggest that these genes are involved in the initial events of plastid biogenesis, and that essential compounds for organ development are produced by the early-developed plastid.…”

“…A gene of tomato, defective chloroplasts and leaves (DCL), which is required for rRNA maturation has been identified in our laboratory. DCL is ubiquitously expressed and encodes a small protein that is required for chloroplast development, palisade cell morphogenesis, and embryogenesis (Keddie et al 1996;Bellaoui et al 2003). Examination of the expression of several nuclear and plastid genes has suggested that DCL protein is involved in the processing of 4.5S rRNA (Bellaoui et al 2003).…”

A chloroplast‐localized PPR protein required for plastid ribosome accumulation

“…This adds to the evidence that the loss of plastid ribosomes, whether induced by mutation or by antibiotics, does not impact leaf cell viability or morphology in the grasses (Han et al, 1993(Han et al, , 1995Hess et al, 1993;Jenkins et al, 1997;Walbot and Coe, 1979;Zubko and Day, 2002). In contrast, there are several examples in dicots in which early blocks in chloroplast biogenesis are accompanied by defects in palisade cell morphogenesis (Chatterjee et al, 1996;Keddie et al, 1996;Reiter et al, 1994;Wang et al, 2000). These observations suggest the possibility that dicot plastid genomes provide a cellular house-keeping function that is provided by a nuclear gene(s) in the grasses.…”

Plastids unleashed: their development and their integration in plant development

“…The equivalent phenotype is observed in a mutant defective in the Arabidopsis DAG-like (DAL ) gene. Similarly a mutation in the tomato DCL (defective chloroplasts and leaves ) gene, necessary for the correct processing of plastidic 4.5 S rRNA (Bellaoui and Gruissem, 2004) lead to the double defect in chloroplasts and in palisade cell morphogenesis that its name indicates (Keddie et al, 1996). Cells, in given cell layers, with ribosome-free plastids can also be generated simply by extended growth on spectinomycin, a plastid translation inhibitor .…”