LEM7, A NOVEL TEMPERATURE-SENSITIVE ARABIDOPSIS MUTATION THAT REVERSIBLY INHIBITS VEGETATIVE DEVELOPMENT

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. D uring vegetative growth in plants, cells in the epical meristem must c oordinate 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 mutatio n that maps to a novel locus on chromosome 2. When grown at 16 degrees C, lem7 reversibly arrests leaf development at the shoot apex. In con trast, lem7 grown at 30 degrees C appears phenotypically normal. Our d ata also suggest that the Lem7 locus may not be involved solely in lea f organogenesis, but may also play a role in floral development and th e maintenance of patterns and structures after cellular differentiatio n. At an intermediate temperature of 23 degrees 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 bila teral symmetry, a rough leaf lamina, a reduced number of trichomes, an d an altered vascular network. Leaves that developed at the permissive temperature (30 degrees C) and shifted to the nonpermissive temperatu re (16 degrees C) form tumor-like outgrowths. Histological analysis of these tumor-like outgrowths and leaves grown at the intermediate temp erature reveal abnormally large mesophyll cells, a disorganized mesoph yll layer, and collapsed epidermal cells. We propose that the reversib le inhibition of leaf development in lem7 under nonpermissive temperat ures may serve as a useful tool for identifying genes involved in Arab idopsis leaf organogenesis. (C) 1996 Academic Press, Inc.