Molecular characterisation of the SNAKESKIN mutation in Arabidopsis
Screening of an En element population of Arabidopsis thaliana resulted in the identification of a mutant known as snakeskin (sks) in which the epidermal cell-cell linkages appear to be significantly perturbed (Marchant and Bennett, unpublished results). As a result of the breakdown of epidermal cell-to-cell linkages there are changes in epidermal cell architecture and distribution. These include alterations in pavement epidermal cell shape, stomatal distribution and trichome morphology. The defect in epidermal cell-to-cell adhesion may be a consequence of reduced cell expansion resulting in increased cell division as a compensation mechanism. This results in altered stomatal index and density and reduced root and hypocotyl elongation. A change in the ability of a cell to expand may be attributed to defects in cell wall composition or to the cytoskeleton that determines where the cell wall components arc localised during expansion. The sks mutant was found to have changes in its cellulose, xyloglucan and pectin fractions of the cell wall resulting in defects in cell wall adhesion, strength and expansion. To gain a greater understanding of the sks mutation the molecular basis of the SKS gene map based cloning was undertaken employing a combination of SSLPs, InDels and SNP markers. The SKS gene was found to be located on the bottom arm of chromosome 1 on BAC clone TIl 111. SALK insert lines have been utilised in a candidate gene approach in addition to fine mapping the mutation with SNP markers.