Session 3: Cell Signalling
Chair: Daphne Preuss, University of Chicago, USA
email: dpreuss@midway.uchicago.edu
Many aspects of plant development are regulated by communication between cells, and several examples were described in the session on cell signalling.
In the Arabidopsis root meristem, initial cells divide in a stereotypical manner to generate the radial pattern of the root. Philip Benfey (New York University) described characterization of two mutations, scarecrow (scr) and short-root (shr), that disrupt the normal division pattern of the initial that generates the root cortex and endodermis. Apparently, SHR is required for endodermal differentiation and SCR for regulation of the longitudinal asymmetric division. SCR encodes a putative transcriptional regulator expressed in the endodermal cell file and in the cortex/endodermal initial. The progressive refinement observed in the SCR expression pattern during root regeneration suggests that radial patterning involves positional information possibly transmitted through cell-cell signalling within the regenerating region.
The development of the Arabidopsis floral meristem is also regulated by cell signalling. A fixed number of floral organs arranged in four concentric whorls is achieved through regulated proliferation and differentiation of meristem cells. Hajime Sakai (Meyerowitz lab, California Institute of Technology) has cloned and analyzed the function of the SUPERMAN (SUP) gene, a putative transcription factor with a zinc finger domain. SUP appears to regulate cell division in whorls that form stamens and carpels, but functions antagonistically in each whorl. In the stamen whorl, SUP functions to repress cell division, but it promotes division in the carpel.
Pollination requires the establishment of cell-cell interactions between male and female cells that do not share a common developmental lineage. Daphne Preuss (University of Chicago) described mutations that provide insight into two stages of pollination: 1) interactions between pollen and stigma cells, and 2) guidance of pollen tubes to ovules. The major pollen surface components consist of a family of oleosin-containing proteins that likely mediate interactions between proteins and lipids at the pollen-stigma interface. Alterations that alter the abundance of lipids and proteins on the pollen surface cause defects in pollen hydration. Subsequent interactions between pollen tubes and pistil cells require the action of at least two genes POP2 and POP3. While expression of these genes in the pistil is sufficient to rescue function of mutant pollen tubes, recent genetic tests indicate that pollen tubes that encode wild-type alleles have a growth advantage over their mutant counterparts.
On the epidermal surface, regulated cell division and cell expansion are required to achieve an organized pattern of stomates, trichomes and root hairs. Fred Sack (Ohio State University) described the cellular interactions that occur during stomatal patterning. Strikingly, wild-type Arabidopsis plants rarely form two stomata in contact with each other. This regular pattern results from the controlled placement of asymmetric cell divisions, such that precursor cells are not formed near existing stomata. The too many mouths mutant forms stomatal clusters that result, in part, from the misplacement of these divisions, causing precursors to form adjacent to existing stomata.
Leaf petioles offer another example of regulated cell expansion. Tony Schaeffner (Ludwig-Maximilians-Universitaet) described tortifolia (tor) mutations that affect morphogenesis of the petiole of Arabidopsis leaves. The mutants have twisted petioles, and curiously, the direction of twisting is gene-specific, with recessive tor1 and tor2 defects causing right-handed torsion, and semi-dominant tor3 defects causing left-handed twisting. Petiole twisting in these mutants is caused by uneven cell expansion, and not by differences in the rates of cell division, and the tor phenotype is not controlled by environmental factors, such as phytohormones, light, or gravity. tor1 maps near to a mutation called spr2 (Takashi Hashimoto, Nara Institute of Science and Technology, Japan) that causes hypocotyl torsion and root slanting.