InPSR42, a putative 14-3-3 protein, regulates petal opening and senescence in Japanese morning glory
The elucidation of the mechanism of petal opening and senescence is important to extend the flower longevity of ornamental crop. Petal opening is caused by cell expansion, which is due to water influx and relaxation of cell-wall strength. Petal senescence is usually classified as a developmental programmed cell death (PCD). These two phenomena are continuous change in petals but it is not still shown clearly how cell expansion and PCD are regulated in petal cells. We have previously isolated genes showing changes in expression during petal opening and senescence (PSRs) in Japanese morning glory (Ipomoea nil 'Violet'). One of the PSRs, InPSR42, of which transcript abundance increased in petals from opening to senescence, encodes a putative 14-3-3 protein. 14-3-3 proteins are being implicated in broad physiological functions, through the regulation of a diverse range of proteins, such as kinases and transcription factors, by binding to phosphorylated client proteins to modulate their function. Transgenic plants reduced InPSR42 expression (42r-lines) showed delay of petal opening, petal wilting, and nuclear fragmentation during petal PCD compared to wild-type plants. RNA-Seq analysis revealed that transcript abundances of cell cycle and membrane maintenance-related genes were changed in the petals of PSR42r plants. These results suggest that InPSR42 acts to induce petal senescence (PCD), possibly through regulation of the cell cycle.
Ono, H., Ishii, K., Kozak, T., Kanekatsu, M., Yamada, T., Shimizu, K., Shibuya, K. and Ichimura, K. (2016). InPSR42, a putative 14-3-3 protein, regulates petal opening and senescence in Japanese morning glory. Acta Hortic. 1120, 105-110
Ipomoea nil, programmed cell death, petal senescence