An important question in developmental biology concerns the mechanisms by which a few cells coordinate division and differentiation to yield the complex structures and organs found in multicellular organisms. During vegetative growth in plants, cells in the apical meristem must coordinate division and differentiation to yield the fully mature leaf organ. Alterations in these processes may result in an abnormal leaf. In this paper we present the isolation and characterization of an EMS-generated, cold-temperature-sensitive mutation in Arabidopsis thaliana designated lem7 (leaf morphogenesis). lem7 is a semidominant mutation that maps to a novel locus on chromosome 2. When grown at 16°C, lem7 reversibly arrests leaf development at the shoot apex. In contrast, lem7 grown at 30°C appears phenotypically normal. Our data also suggest that the Lem7 locus may not be involved solely in leaf organogenesis, but may also play a role in noral development and the maintenance of patterns and structures after cellular differentiation. At an intermediate temperature of 23°C, leaves on the lem7 plant emerged phenotypically normal but began to show drastic changes at about 13 days postgermination. These changes include a reduced bilateral symmetry, a rough leaf lamina, a reduced number of trichomes, and an altered vascular network. Leaves that developed at the permissive temperature (30°C) and shifted to the nonpermissive temperature (16°C) form tumor-like outgrowths. Histological analysis of these tumor-like outgrowths and leaves grown at the intermediate temperature reveal abnormally large mesophyll cells, a disorganized mesophyll layer, and collapsed epidermal cells. We propose that the reversible inhibition of leaf development in lem7 under nonpermissive temperatures may serve as a useful tool for identifying genes involved in Arabidopsis leaf organogenesis.
CITATION STYLE
Meisel, L., Xie, S., & Lam, E. (1996). lem7, a novel temperature-sensitive Arabidopsis mutation that reversibly inhibits vegetative development. Developmental Biology, 179(1), 116–134. https://doi.org/10.1006/dbio.1996.0245
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