biology
Vol 455 | 11 September 2008 | doi:10.1038/nature07271
ARTICLES
Strigolactone inhibition of shoot branching
`
Victoria Gomez-Roldan1, Soraya Fermas2, Philip B. Brewer3, Virginie Puech-Pages1, Elizabeth A. Dun3,
Jean-Paul Pillot2, Fabien Letisse4, Radoslava Matusova5, Saida Danoun1, Jean-Charles Portais4,
´
Harro Bouwmeester5,6, Guillaume Becard1, Christine A. Beveridge3,7*, Catherine Rameau2* & Soizic F. Rochange1*
A carotenoid-derived hormonal signal that inhibits shoot branching in plants has long escaped identification. Strigolactones are compounds thought to be derived from carotenoids and are known to trigger the germination of parasitic plant seeds and stimulate symbiotic fungi. Here we present evidence that carotenoid cleavage dioxygenase 8 shoot branching mutants of pea are strigolactone deficient and that strigolactone application restores the wild-type branching phenotype to ccd8 mutants.
Moreover, we show that other branching mutants previously characterized as lacking a response to the branching inhibition signal also lack strigolactone response, and are not deficient in strigolactones. These responses are conserved in Arabidopsis.
In agreement with the expected properties of the hormonal signal, exogenous strigolactone can be transported in shoots and act at low concentrations. We suggest that endogenous strigolactones or related compounds inhibit shoot branching in plants. Furthermore, ccd8 mutants demonstrate the diverse effects of strigolactones in shoot branching, mycorrhizal symbiosis and parasitic weed interaction.
More than a decade ago, increased branching mutants in garden pea
(Pisum sativum L.) and petunia (Petunia hybrida), rms1 and dad1 respectively, revealed that a mobile signal produced in shoot and root inhibits shoot branching1,2. For simplicity, we refer to this signal as SMS
(shoot multiplication signal)3. SMS moves acropetally in shoots and inhibits lateral bud outgrowth4. On the basis of measurements of
ARTICLES
Strigolactone inhibition of shoot branching
`
Victoria Gomez-Roldan1, Soraya Fermas2, Philip B. Brewer3, Virginie Puech-Pages1, Elizabeth A. Dun3,
Jean-Paul Pillot2, Fabien Letisse4, Radoslava Matusova5, Saida Danoun1, Jean-Charles Portais4,
´
Harro Bouwmeester5,6, Guillaume Becard1, Christine A. Beveridge3,7*, Catherine Rameau2* & Soizic F. Rochange1*
A carotenoid-derived hormonal signal that inhibits shoot branching in plants has long escaped identification. Strigolactones are compounds thought to be derived from carotenoids and are known to trigger the germination of parasitic plant seeds and stimulate symbiotic fungi. Here we present evidence that carotenoid cleavage dioxygenase 8 shoot branching mutants of pea are strigolactone deficient and that strigolactone application restores the wild-type branching phenotype to ccd8 mutants.
Moreover, we show that other branching mutants previously characterized as lacking a response to the branching inhibition signal also lack strigolactone response, and are not deficient in strigolactones. These responses are conserved in Arabidopsis.
In agreement with the expected properties of the hormonal signal, exogenous strigolactone can be transported in shoots and act at low concentrations. We suggest that endogenous strigolactones or related compounds inhibit shoot branching in plants. Furthermore, ccd8 mutants demonstrate the diverse effects of strigolactones in shoot branching, mycorrhizal symbiosis and parasitic weed interaction.
More than a decade ago, increased branching mutants in garden pea
(Pisum sativum L.) and petunia (Petunia hybrida), rms1 and dad1 respectively, revealed that a mobile signal produced in shoot and root inhibits shoot branching1,2. For simplicity, we refer to this signal as SMS
(shoot multiplication signal)3. SMS moves acropetally in shoots and inhibits lateral bud outgrowth4. On the basis of measurements of