Thursday, June 09, 2011
KBC-Days 2009
All day
The KBC Days 2009 will take place on 16-17 November 2009
All members of the KBC-Departments are welcome to two days of communication, celebration and inspiration. We cordially invite our research partners and friends who like to learn more about our centre.
Read more ...
All members of the KBC-Departments are welcome to two days of communication, celebration and inspiration. We cordially invite our research partners and friends who like to learn more about our centre.
Read more ...
Seminar - Dr Angus Murphy
Thu. 9 Jun, 2011 15:00 - 16:00
Title: Darwin had it right: phototropic auxin relocalization is conserved between dicots and monocots
Lecturer: Dr Angus Murphy, Department of Horticulture, Purdue University, USA
Place: KB3B3, KBC
Abstract: Plants depend on sunlight for photosynthesis and adjust their growth to optimize light capture. Phototropism, the reorientation of growth toward light, is one of the most important of these adaptive processes. Originally identified in grass coleoptiles by Charles and Francis Darwin, phototropism is initiated by light perceived at the shoot tip to generate a diffusible signal that influences differential elongation in the tissues below. Subsequent studies have shown that phototropism arises from increased growth on the shaded side of the stem, owing to an accumulation of the phytohormone auxin.
Research from the past two decades has identified and characterized the PHOTOTROPIN (PHOT) blue light receptors as the primary receptors that modulate phototropic curvatures in the model plant Arabidopsis. Downstream signalling effectors are assumed to act on auxin transport proteins from the PIN, AUX1/LAX, and ABCB families to control directional auxin movement.
However, somewhat surprisingly, it is still not clear how these receptor mechanisms actually control auxin movement in the shoot apex and what the exact path of auxin movement is in. We have established a system in Arabidopsis to study hypocotyl phototropism in the absence of developmental events associated with seedling photomorphogenesis and hook opening. Using this system, we have shown that auxin redistribution to epidermal sites of action occurs at the hypocotyl apex in dicots as is the case in monocots, not out of the vascular cylinder in the hypocotyl elongation zone as has been assumed for the past decade.
Within this region, we identified the auxin efflux transporter ATP-BINDING CASSETTE B19 (ABCB19) as the first substrate target for the photoreceptor kinase PHOTOTROPIN1(PHOT1). In vivo and in vitro analyses showed that phosphorylation of ABCB19 by PHOT1 inhibits ABCB19 efflux activity and increases auxin levels in the cotyledonary node to halt vertical growth and prime lateral fluxes that are subsequently channeled to the elongation zone by PIN3. These results demonstrate that the proximity of light perception and differential phototropic growth is conserved in angiosperms, but also demonstrated that no single or viable double or triple mutant in known auxin transporters bends phototropically. As no new non-bending mutant has been identified in the many screens for phototropism mutants over the past decade, either a missing component of the process that mediates auxin redirection is essential for viability, or the full complement of transporters that function in lateral auxin redistribution has not been discovered. In any case, the widely held perception that the mechanism underlying lateral redistribution of auxin in phototropism has been resolved is not supported by substantive data.
Lecturer: Dr Angus Murphy, Department of Horticulture, Purdue University, USA
Place: KB3B3, KBC
Abstract: Plants depend on sunlight for photosynthesis and adjust their growth to optimize light capture. Phototropism, the reorientation of growth toward light, is one of the most important of these adaptive processes. Originally identified in grass coleoptiles by Charles and Francis Darwin, phototropism is initiated by light perceived at the shoot tip to generate a diffusible signal that influences differential elongation in the tissues below. Subsequent studies have shown that phototropism arises from increased growth on the shaded side of the stem, owing to an accumulation of the phytohormone auxin.
Research from the past two decades has identified and characterized the PHOTOTROPIN (PHOT) blue light receptors as the primary receptors that modulate phototropic curvatures in the model plant Arabidopsis. Downstream signalling effectors are assumed to act on auxin transport proteins from the PIN, AUX1/LAX, and ABCB families to control directional auxin movement.
However, somewhat surprisingly, it is still not clear how these receptor mechanisms actually control auxin movement in the shoot apex and what the exact path of auxin movement is in. We have established a system in Arabidopsis to study hypocotyl phototropism in the absence of developmental events associated with seedling photomorphogenesis and hook opening. Using this system, we have shown that auxin redistribution to epidermal sites of action occurs at the hypocotyl apex in dicots as is the case in monocots, not out of the vascular cylinder in the hypocotyl elongation zone as has been assumed for the past decade.
Within this region, we identified the auxin efflux transporter ATP-BINDING CASSETTE B19 (ABCB19) as the first substrate target for the photoreceptor kinase PHOTOTROPIN1(PHOT1). In vivo and in vitro analyses showed that phosphorylation of ABCB19 by PHOT1 inhibits ABCB19 efflux activity and increases auxin levels in the cotyledonary node to halt vertical growth and prime lateral fluxes that are subsequently channeled to the elongation zone by PIN3. These results demonstrate that the proximity of light perception and differential phototropic growth is conserved in angiosperms, but also demonstrated that no single or viable double or triple mutant in known auxin transporters bends phototropically. As no new non-bending mutant has been identified in the many screens for phototropism mutants over the past decade, either a missing component of the process that mediates auxin redirection is essential for viability, or the full complement of transporters that function in lateral auxin redistribution has not been discovered. In any case, the widely held perception that the mechanism underlying lateral redistribution of auxin in phototropism has been resolved is not supported by substantive data.