Alower concentration of Strigolactones in the plants treated with inhibitors ofcarotenoid biosynthesis and total nonappearance of strigolactones in carotenoid insufficient mutants put forward for thought thatstrigolactones were inferred from carotenoids.A widecollection of shoot branching mutants that were deficient in strigolactones biosynthesisor signalling helped to understand and define the assembly of strigolactonesbiosynthesis and signalling pathways and lead to a proposed strigolactones biosynthesispathway. These branching mutants are 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.
The advanceddiscovery of regulation of shoot branching and tillering by strigolactonesexhibited that the two carotenoid cleavage dioxygenases(CCDs), CCD7 and CCD8,encoded by MAX3/RMS5/D17(HTD1)/DAD3 and MAX4/RMS1/D10/DAD1 respectively. Theses CCDs catalysesthe oxidative cleavage of carotenoid double bonds to release carbonyl productscalled apocarotenoids. The excusivesubstrate for strigolactones biosynthesis is trans-?-carotene.
The plants a stereo-selective enzyme lycopene- ?-cyclase, catalyse the conversion of ?-carotene forms to all-trans-configured ?-carotene. These trans-configured – ?-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 strigolactone-likecompound named Carlactone (CL), which is an intermediated compound in the SLpathway containing only A and D rings with enol ether bridge (Alder et al., 2012). Cytochrome P450 of theCYP711A1clade encoded by MAX1 in Arabidopsis is responsible for the conversionof Carlactone into functional SLs such as 5-deoxystrigol (Stirnberg et al., 2002; Booker et al.
, 2004; Alder et al., 2012). Therearrangements and modifications (hydroxylation, oxidation) caused by MAX1,converts Carlactone to carlactonic acid (CLA) then further transformed tomethyl carlactonoate (MeCLA) by an unknown enzyme (Abe et al., 2014). In rice,one MAX1 paralogue converts carlactone into ent-20-epi-5-deoxystrigol, thepresumed precursor of rice SL.
