Chi-Lien Cheng Ph.D.
chi-lien-cheng
uiowa
edu
Associate Professor of Biological Sciences
My laboratory studies the molecular mechanisms by which environmental signals are incorporated into the growth and developmental program of plants. We concentrate on two aspects, greening and senescence of the leaves. Greening occurs at the beginning of leaf development and senescence precedes the death of a leaf. Both greening and senescence are regulated by internal factors, such as hormones and sugar levels, as well as by environmental factors, such as light. We use a combination of classical genetics, molecular cloning technologies, and biochemistry to identify genes regulating these developmental processes. The overriding strategy in these studies is to isolate mutants defective in these processes, and use these mutants as inroads to understand the developmental programs leading to greening and senescence. Arabidopsis thaliana is our model organism. Arabidopsis is well suited for genetic analysis. The genetic and physical maps of the Arabidopsis genome are well integrated and its sequence is completed. This facilitates cloning the gene of interest. Once the genes are cloned, we can employ molecular technologies to examine the regulation of the gene's expression, the biochemical function of the protein it encodes, and the developmental and physiological roles of the protein. The characterization of mutants in greening and senescence is described briefly below. We have identified mutants defective in greening. One of these, cr88, has been characterized and the affected gene cloned. The CR88 gene encodes for a chloroplast-targeted HSP90 molecular chaperone. We are using biochemistry to identify cochaperones that interact with CR88 and genetics to identify the client proteins that require the CR88 chaperone function to mature. To study the senescence process, we isolated mutants that are delayed in this process. One such mutant, sds1, has been characterized. The sds1 mutant exhibits delays in both natural and artificially induced senescence (see figure). In addition, the mutant is less sensitive to sugar levels. The delays in visible phenotypes correlate with delays in the down-regulation of photosynthetic gene expression and in the up-regulation of senescence marker gene expression. We have mapped the SDS1 locus to the North arm of chromosome 1 and are in the process of cloning the gene. The identity of the SDS1 protein will provide vauable information about the interplay of sugar sensing and senescence. The combination of genetic, molecular biological, and biochemical studies will allow us to understand certain aspects of the greening process and the control of senescence during plant development.
Selected Publications
Escamilla, L.L.E., Chen, W., Card, M.L., Shih, M.-C. Cheng, C.-L., and Poulton, J.E. (2006) Arabidopsis thaliana b-glucose BGLU45 and BGLU46 hydrolyse monolignol glucosides. Phtochem. (in press, accepted May 15, 2006).
Xu, Z., Escamilla, L.L.E., Zheng L., Lalgondar, M., Bevan, D.R., Mohamed, A., Cheng, C.-L., Shih, M.-C., Poulton, J.E., and Esen, A. (2004) Functional genomic analysis of Arabidopsis thaliana glycoside hydrolase family 1. (in press, Plant Mol. Biol.)
Cao, D., Froehlich, J.E., Zhang, H., and Cheng, C.-L. (2003) A photomorphogenesis defective mutant cr88 encodes a chloroplast Hsp90. Plant J 33: 107-118. Stanislaus M.A. and Cheng, C.-L. (2002) Genetically engineered self-destruction: an alternative to herbicides for cover crop systems. Weed Sci. 50: 794-801.
Cao, D., Lin, Y., and Cheng, C.-L. (2000) Genetic interactions between chlorate resistant mutant cr88 and photomorphogenic mutants cop1 and hy5. Plant Cell 12: 199-210.
Lin, Y. and Cheng, C.-L. 1997. A chlorate-resistant mutant defective in the regulation of nitrate reductase gene expression in Arabidopsis defines a new HY locus. Plant Cell 9: 21-35.
Hwang, C.-F., Lin, Y., D'Souza, T.S., and Cheng, C.-L. 1997. Molecular analyses of nitrate-induced transcription of the Arabidopsis nitrate reductase genes. Plant Physiol. 113: 853-862.
