lack of strigolactones in carotenoid-deficient mutants and the reduced levels
of strigolactones in exudates of plants treated with inhibitors of carotenoid
biosynthesis suggested that strigolactones are derived from carotenoids.
A wide collections of branching
mutants are in Arabidopsis thaliana known as more axillary growth (max)
mutants, Oryza sativa dwarf (d) or high-tillering dwarf or (htd) mutants,
Pisum sativum ramosus (rms) mutants and Petunia hybrida decreased apical
dominance (dad) mutants All
these mutants are defective in SL biosynthesis or signaling. Anaysis of
these mutants helped to understand and define most of the current assembly of
SL biosynthetic (and signaling) pathways and to a hypothetical SL-biosynthetic
pathway was proposed.
The breakthrough discovery of the role of strigolactones in
the regulation of shoot branching and tillering revealed that two carotenoid
cleavage dioxygenases (CCDs), CCD7 and CCD8, encoded by MAX3/RMS5/D17(HTD1)/DAD3 and MAX4/RMS1/D10/DAD1 respectively, are involved in the proposed
carotenoid cleavage. These CCDs catalyse the oxidative cleavage of carotenoid double bonds,
yielding carbonyl products called apocarotenoids.
The plant enzyme lycopene-b-cyclase, is a stereo-selective enzyme
which catalyzes the synthesis of b-carotene to exclusively form all-trans-configured b-carotene. These trans-?-carotene are converted into 9-cis-?-carotene
(C-40) by the activity of
?-carotene isomerase, encoded by D27 in Arabidopsis. The later acts as substrate
for CCD7 which cleaves cis-configured carotenoids into 9-cis-?- apo-10′-carotenal (C-27) and ?-ionone (C-13) (Schwartz et al., 2004; Alder et al., 2012; Waters et al., 2012a).
CCD8 then acts on the 9-cis-?-apo-10′-carotenal
product of enzymatic cleavage to form a SL-like compound named Carlactone (CL),
which is an intermediated compound in the SL pathway containing only A and D
rings with enol ether bridge (Alder et al.,
2012). Cytochrome P450 of the CYP711A1clade
encoded by MAX1 in Arabidopsis is responsible for the conversion of CL into
functional SLs such as 5-deoxystrigol (Stirnberg et al., 2002; Booker et al., 2004; Alder et al., 2012). The rearrangements and modifications (hydroxylation,
oxidation) caused by MAX1, converts CL to carlactonic acid (CLA) then further
transformed to methyl carlactonoate (MeCLA) by an unknown enzyme (Abe et al., 2014). In rice,
one MAX1 paralogue converts carlactone into ent-20-epi-5-deoxystrigol, the
presumed precursor of rice SL.