When subjected to variation in temperature, light, wind, or humidity, plants alter their physiology and development. Environmental conditions influence commitment to developmental events such as seed germination and flowering, as well as adjustments of growth leading to morphological variation, such as stem elongation, lateral bud inhibition (apical dominance), and leaf size. This plasticity of plant growth and form enables one to learn about the mechanisms of plant development by studying signal transduction pathways that link environmental signals to developmental responses. This proposal describes experiments designed to elucidate molecular mechanisms of light signal transduction. Light influences virtually all aspects of plant development, through signalling system distinct from the photosynthetic apparatus. These systems respond to far-red, red, blue, or UV light through the action of distinct photoreceptors. Mutations in the PHYB gene, encoding the red/far-red photoreceptor phytochrome B, cause several developmental phenotypes including elongated hypocotyls, early flowering, and increased apical dominance. Characterization of more phyB mutations will provide information on structural requirements for phytochrome B function. Screens for mutations that suppress or enhance the long hypocotyl phenotype of a phyB mutant will identify genes whose products function downstream in phytochrome B signal transduction, and possibly, in other light signalling pathways. Genetic and physiological experiments will reveal the roles of genes identified by the mutations in control of development by light. Map-based cloning of the most interesting loci will permit molecular reconstruction of the pathways controlling plant developmental responses to the environment. Understanding these mechanisms may allow more rational manipulation of agronomically important traits such as flowering, seed, germination, and height in crop plants, contributing to improvement in human nutrition. These experiments will also lead to fuller insight into basic mechanisms of plant growth.

Agency
National Institute of Health (NIH)
Institute
National Institute of General Medical Sciences (NIGMS)
Type
First Independent Research Support & Transition (FIRST) Awards (R29)
Project #
5R29GM052456-04
Application #
2701665
Study Section
Molecular Biology Study Section (MBY)
Project Start
1995-05-01
Project End
2000-04-30
Budget Start
1998-05-01
Budget End
1999-04-30
Support Year
4
Fiscal Year
1998
Total Cost
Indirect Cost
Name
University of North Carolina Chapel Hill
Department
Biology
Type
Schools of Arts and Sciences
DUNS #
078861598
City
Chapel Hill
State
NC
Country
United States
Zip Code
27599
Ploense, Sara E; Wu, Miin-Feng; Nagpal, Punita et al. (2009) A gain-of-function mutation in IAA18 alters Arabidopsis embryonic apical patterning. Development 136:1509-17
Tian, Qing; Uhlir, Nicholas J; Reed, Jason W (2002) Arabidopsis SHY2/IAA3 inhibits auxin-regulated gene expression. Plant Cell 14:301-19
Elumalai, Rangasamy P; Nagpal, Punita; Reed, Jason W (2002) A mutation in the Arabidopsis KT2/KUP2 potassium transporter gene affects shoot cell expansion. Plant Cell 14:119-31
Nagpal, P; Walker, L M; Young, J C et al. (2000) AXR2 encodes a member of the Aux/IAA protein family. Plant Physiol 123:563-74
Krall, L; Reed, J W (2000) The histidine kinase-related domain participates in phytochrome B function but is dispensable. Proc Natl Acad Sci U S A 97:8169-74
Reed, J W; Nagpal, P; Bastow, R M et al. (2000) Independent action of ELF3 and phyB to control hypocotyl elongation and flowering time. Plant Physiol 122:1149-60
Reed, J W (1999) Phytochromes are Pr-ipatetic kinases. Curr Opin Plant Biol 2:393-7
Reed, J W; Elumalai, R P; Chory, J (1998) Suppressors of an Arabidopsis thaliana phyB mutation identify genes that control light signaling and hypocotyl elongation. Genetics 148:1295-310