Trichome cell growth in Arabidopsis thaliana can be derepressed by mutations in at least five genes.
Leaf trichomes in Arabidopsis are unicellular epidermal hairs with a branched morphology. They undergo successive endoreduplication rounds early during cell morphogenesis. Mutations affecting trichome nuclear DNA content, such as triptychon or glabra3, alter trichome branching. We isolated new mutants with supernumerary trichome branches, which fall into three unlinked complementation groups: KAKTUS and the novel loci, POLYCHOME and RASTAFARI. They map to chromosomes IV, II, and V, respectively. The trichomes of these mutants presented an increased DNA content, although to a variable extent. The spindly-5 mutant, which displays a constitutive gibberellin response, also produces overbranched trichomes containing more nuclear DNA. We analyzed genetic interactions using double mutants and propose that two independent pathways, defined by SPINDLY and TRIPTYCHON, act to limit trichome growth. KAKTUS and POLYCHOME might have redundant actions mediating gibberellin control via SPINDLY. The overall leaf polysomaty was not notably affected by these mutations, suggesting that they affect the control of DNA synthesis in a tissue- or cell type-specific manner. Wild-type tetraploids also produce overbranched trichomes; they displayed a shifted polysomaty in trichomes and in the whole leaf, suggesting a developmental program controlling DNA increases via the counting of endoreduplication rounds.
Perazza
D
D
Laboratoire de Génétique Moléculaire des Plantes, CNRS-Université J. Fourier, 38041 Cedex 9, Grenoble, France.
Herzog
M
M
Hülskamp
M
M
Brown
S
S
Dorne
A M
AM
Bonneville
J M
JM
D000483:Alleles; D017360:Arabidopsis / Q000235:genetics* / Q000378:metabolism; D002455:Cell Division / Q000235:genetics*; D002874:Chromosome Mapping; D004247:DNA / Q000032:analysis / Q000378:metabolism; D004252:DNA Mutational Analysis; D005434:Flow Cytometry; D005816:Genetic Complementation Test; D008040:Genetic Linkage; D008856:Microscopy, Fluorescence; D008957:Models, Genetic; D016296:Mutagenesis; D010641:Phenotype; D012097:Repressor Proteins / Q000378:metabolism
D012097:Repressor Proteins; D004247:DNA