Jennifer Normanly
Associate Professor of Biochemistry and Molecular Biology, University of Massachusetts

Email:
normanly@biochem.umass.edu
Normanly Lab Web Page

Ph.D.: California Institute of Technology
Postdoctoral Training: The Whitehead Institute for Biomedical Research


Auxin Biosynthesis and High Throughput Metabolic Profiling

A central aspect to signal transduction is the regulation of the signaling molecule itself. Genetic approaches, in the form of simple visual screens for phenotypes that indicate aberrant signaling, have been very useful in a variety of systems to identify components of a signaling pathway. Complex, redundant pathways are less amenable to simple visual screens because defects in one pathway are often compensated for by another functional pathway.

My laboratory is developing high throughput metabolic profiling assays in order to screen for mutants in complex regulatory pathways. Our model system is the small flowering plant, Arabidopsis thaliana, and we are characterizing the regulation of the signaling molecule, auxin. Auxin is fundamentally important in plant growth and development as a regulator of numerous biological processes. The primary plant auxin, indole-3-acetic acid (IAA) is tightly regulated through a network of redundant pathways, including biosynthesis, inactivation, transport and signal transduction. In piecing together these pathways, a variety of visual screens have identified candidate genes, but there are many more genes that have yet to be identified.

As part of a NSF-sponsored Plant Genome Initiative, our lab is part of a consortium working to identify mutants that are involved in all aspects of auxin biology. My laboratory is part of a team that is developing a sensitive screen for mutants with small changes in IAA levels. Using automated sample handling and mass spectral quantification we can identify mutants with defects in redundant pathways that would not be detected in a simple visual screen. Sequence information is currently available for the entire Arabidopsis genome, so identifying the genes that correspond to these mutants will be straightforward. Transgenic technology is also simple in Arabidopsis, so any candidate genes can be re-introduced into Arabidopsis in a variety of formats (antisense, overexpression, inducible expression, tissue-specific expression) in order to test their function.


Representative publications:

Brown, D.E., Rashotte, A. M., Murphy, A. S., Normanly, J., Tague, B. W., Peer, W. A., Taiz, L., and Muday, G. K. (2001) Flavonoids act as negative regulators of auxin transport in vivo in Arabidopsis thaliana. Plant Physiology (in press)

Tam, Y. Y, Epstein, E. and Normanly, J. (2000) Characterization of auxin conjugates in Arabidopsis. Low steady-state levels of indole-3-acetyl-aspartate, indole-3-acetyl-glutamate, and indole-3-acetyl-glucose. Plant Physiology 123:589-595

Normanly, J. and Bartel, B. (1999) Redundancy as a way of life: IAA metabolism. Current Opinion in Plant Biology 2, 207-213.

Quirino, B., Normanly, J. and Amasino, R. M. (1999) Diverse range of gene activity during Arabidopsis thaliana leaf senescence includes pathogen-independent induction of defense-related genes. Plant Molecular Biology 40:267-278.

Tam, Y. Y. and Normanly, J. (1998) Determination of indole-3-pyruvic acid levels in Arabidopsis thaliana by gas chromatography-mass spectrometry. Journal of Chromatography A 800, 101-108.

Normanly, J., Grisafi, P., Fink, G. R., and Bartel, B. (1997) Arabidopsis thaliana mutants resistant to the auxin effects of indole-3-acetonitrile are defective in the nitrilase encoded by the NIT1 gene. The Plant Cell 9, 1781-1790.

Normanly, J (1997) Auxin Metabolism. Physiologia Plantarum 100, 431-442.

Normanly, J., Slovin, J. P., and Cohen, J. D. (1995) Rethinking IAA metabolism. Plant Physiology 107, 323-329.

Normanly, J., Cohen, J.D., and Fink, G.R. (l993) Arabidopsis thaliana auxotrophs reveal a tryptophan-independent biosynthetic pathway for indole-3-acetic acid. Proc. Natl. Acad. Sci. (USA) 90, 10355-10359.


Revised: 2/01