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PhD Exit Seminar – Duncan Holbrook-Smith (McCourt lab)

September 26, 2016 @ 1:10 pm - 2:10 pm

PhD Exit Seminar

Monday September 26th, 1:10 pm – Ramsay Wright Building, Rm. 432


Duncan Holbrook-Smith (McCourt lab)


“Chemical Genetic Interrogation of Strigolactone Receptors in Arabidopsis and Striga hermonthica





Strigolactones are a class of terpenoid plant hormones that regulate various areas of plant growth and development. They are best known as suppressors of axillary growth, but have also been implicated in areas as diverse as leaf shape, hypocotyl length, and seed germination. However, parasitic plants of the genera Striga, Orobanche, and Phelipanche have evolved to use strigolactones released from host plant roots as a cue for germination and parasitism. Because these parasitic plants cause billion-dollar yield losses in the developing world each year, considerable research efforts have been dedicated towards understanding the mechanism of strigolactone perception.


The alpha/beta hydrolase HTL is the receptor for strigolactones in the seed. HTL interacts with effector proteins to elicit a strigolactone response. HTL-dependent signaling leads to increased germination and reduced hypocotyl length. We decided to use a chemical genetic approach to both probe HTLs while also developing Striga control technologies. Separately, we screened approximately 4000 compounds from a chemical library to identify small molecules that could be agonists and antagonists for Arabidopsis HTL. We were able to show that many of the compounds we isolated from the chemical screen were able to directly bind to HTL, and their action was specific to strigolactone signaling. These compounds were also able to stimulate Striga hermonthica germination, showing they have promise as leads for Striga control technology development.


In order to identify new genes involved in strigolactone signaling, we screened a collection of overexpression lines for the ability to resist the effects of an HTL antagonist on germination. We found that the overexpression of the splicing factor U2AF35B was sufficient to suppress the effect of an antagonist on germination, and could partially suppress phenotypes associated with loss-of-function alleles of HTL. This suggests that U2AF35B plays a role in strigolactone signaling at or downstream of HTL.

Ramsay Wright is a wheelchair accessible building.




September 26, 2016
1:10 pm - 2:10 pm
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Ramsay Wright Building, Room 432
25 Harbord St.
Toronto, ON M5S 3G5 Canada