Elizabeth A. Dun

TL;DR: Evidence is presented 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, and that other branching mutants previously characterized as lacking a response to the branching inhibition signal also lack striglactone response.

TL;DR: Karrikin signaling requires the F-box protein MAX2, which also mediates responses to the structurally-related strigolactone family of phytohormones, and it is shown that plants can distinguish between these signals.

TL;DR: It is found that exogenously applied strigolactone inhibited bud outgrowth in pea (Pisum sativum) even when auxin was depleted after decapitation, suggesting that auxin may act through strigsolactones to facilitate apical dominance.

TL;DR: It is found that SL-deficient plants are more sensitive to stimulation of bud growth by low concentrations of locally applied CK than wild-type plants and the expression of pea BRANCHED1, a TCP transcription factor expressed strongly in buds and thought to act downstream of SLs in shoot branching, is regulated by CK and SL in a manner that correlates with observed bud growth responses.

TL;DR: In this article, the authors provide physiological, genetic, and pharmacological evidence that strigolactones (SLs), a group of plant hormones recently described to be involved in the repression of shoot branching, positively regulate cambial activity.