Tomato UVI4 and CCS52B play important roles in hypocotyl elongation via
modulation of cell cycle progression
Abstract
Tomato hypocotyl elongation is a consequence of active cell division and
expansion, both of which require precisely regulated cell cycle
progression. Little is known about the function of APC/C regulators in
cell cycle progression during hypocotyl growth. Here, we isolated and
characterized the positive and negative APC/C regulators, SlCCS52 and
SlUVI4 genes in tomato. We probed SlUVI4 and SlCCS52B roles in tomato
hypocotyl elongation via modulating cell cycle progression. Light
especially blue light represses the transcription of SlUVI4 and SlCCS52B
to inhibit the hypocotyl elongation through the suppression of
endoreduplication. MS basal salts and sugar both improve SlUVI4 and
SlCCS52B transcription to enhance hypocotyl length via the promotion of
endoreduplication. Hypocotyl elongation enhanced by heat might require
auxin-induced repression of SlUVI4 transcription. Salt inhibits
hypocotyl elongation possibly through ethylene-mediated modulation of
SlUVI4 and SlCCS52B transcription. Genetic studies reveal that tomato
deletion mutant of SlUVI4 and overexpression plants of SlCCS52B in
Arabidopsis both exhibit shorter hypocotyl with enhanced
endoreduplication. Thus, our results suggest that APC/C activities
stimulated by SlCCS52 genes requires SlUVI4-meidated inhibitory
machinery to reorchestrate cell cycle progression and facilitate
hypocotyl elongation.