Strigolactone defective mutants of Arabidopsis exhibit delayed sepal senescence
Xu, X.; Jibran, R.; Wang, Y.; Dong, L.; Flokova, K.; Esfandiari, A.; McLachlan, A.; Heiser, A.; Sutherland-Smith, A.; Bouwmeester, H. J.; Dijkwel, P.; Hunter, D. A.
Show abstract
Flower sepals are critical for flower development and vary greatly in lifespan depending on their function postpollination. However, very little is known on what controls sepal longevity. Using a sepal senescence mutant screen, we directly connected strigolactones (SL) with sepal longevity. We identified two Arabidopsis mutants that harbour novel mutations in the SL biosynthetic gene MORE AXILLARY GROWTH1 (MAX1) and receptor DWARF14 (AtD14). The mutation in AtD14 caused a substitution of the catalytic Ser-97 to Phe in the enzyme active site. The lesion in MAX1 changed a highly conserved Gly-469 to Arg in the haem-iron ligand signature of the cytochrome P450 protein, which caused loss-of-function of MAX1. nCounter-based transcriptional analysis suggested an interaction between SL and sugar signalling in controlling dark-induced inflorescence senescence. The results uncover an important function for SL in regulating floral organ senescence in addition to its other diverse functions in plant development and stress response. One-sentence summaryTwo novel mutants in the strigolactone pathway demonstrate a role for the hormone in sepal senescence, and transcriptional analysis highlights interaction between strigolactones and sugar signalling.
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