Kodama, K., et al. · 2022 · Nature Communications research
doi:10.1038/s41467-022-31708-3 PMID:35803942 PMC9270392
| Gene ID | Name | Evidence / Role | Function (this paper) |
|---|---|---|---|
| — | MpCCD8 missing | experimental subject | CRISPR knockout of the two paralogs (ccd8a/8b) abolished carlactonoic acid and bryosymbiol (BSB) accumulation, confirming MpCCD8 as the core carotenoid-cleavage enzyme initiating strigolactone biosynthesis. Double mutants showed no or very few arbuscular mycorrhizal infection sites, while single mutants colonized normally, establishing that BSB is essential as an exuded rhizosphere symbiotic signal. |
| — | MpMAX1 missing | experimental subject | CRISPR knockout (max1) and yeast microsomal assays showed MpMAX1 converts carlactone to carlactonoic acid and on to BSB; mutants lost BSB and accumulated carlactone. Acts as the downstream cytochrome P450 in the BSB biosynthetic pathway. |
| Mp5g09160 | MpDLP1 missing | experimental tool | Used as a KAI2-dependent transcriptional marker; qRT-PCR showed GR24 induction only in AtD14-overexpressing lines, not WT. |
| Mp3g06310 | MpSMXL | experimental tool | Used as a KAI2-dependent signaling marker; transcript induced by GR24 enantiomers in AtD14ox lines in a concentration-dependent manner. |
| Mp2g11710 | MpKAI2A | experimental background | CRISPR knockout caused developmental defects (reduced upward thallus growth, delayed gemma cup initiation); DSF showed only weak (−)-GR24 binding. A KAI2-clade receptor governing development, not BSB perception. |
| Mp2g04930 | MpKAI2B | experimental background | CRISPR knockout of this KAI2 paralog; DSF detected no interaction with GR24. Not a receptor for endogenous BSB, supporting that Marchantia lacks a cognate strigolactone hormone receptor. |
| Mp1g02580 | MpMAX2 | experimental background | CRISPR knockout produced developmental defects resembling kai2a mutants with no altered strigolactone levels; an F-box component of KAI2-dependent signaling unconnected to BSB metabolism. |