Tomato UVI4 and CCS52B play important roles in hypocotyl elongation via modulation of cell cycle progression

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.