Abstract:
Endoreplication, also known as endoreduplication, is a phyogenetically widespread modified version of
the cell cycle in which DNA replication is not followed by cell division. The SIAMESE (SIM) gene of
Arabidopsis thaliana encodes the founding member of a novel class of plant-specific cyclin-dependent
kinase (CDK) inhibitors and is a key regulator of endoreplication during the development of trichomes
(shoot epidermal hairs). Here, we have identified mutations in the CCS52A1 gene as genetic modifiers of
the multicellular trichome phenotype of sim mutants. Loss-of-function ccs52A1 mutations dramatically
enhance the multicellularity of sim mutants trichomes in double mutants, whereas overexpression of
CCS52A1 completely suppresses the sim mutant phenotype. CCS52A1 encodes a CDH1/FZR-like protein, a
class of proteins that function as activators of the anaphase-promoting complex. Unicellular ccs52A1
trichomes become multicellular upon overexpression of B-type cyclin, consistent with repression of the
accumulation of mitotic cyclins in the developing trichome by CCS52A1. As these M-phase-specific cyclins
are known to accumulate in sim mutant trichomes, our data suggest that CCS52A1 and SIM cooperate in
repressing accumulation of mitotic cyclins to establish the trichome endocycle. Comparison with endoreplication
pathways in Drosophila and mammals indicates that while these organisms all use similar
components to initiate endoreplication, the components are deployed differently in each organism.
