Institute for Integrative Genome Biology

• A to Z Listing
• Campus Map
• Help

Xuemei Chen

Professor

Mailing Address:

Botany and Plant Sciences
Batchelor Hall /1125
University of California
Riverside, CA 92521

Phone: (951) 827-3988
Fax: (951) 827-4294
Email: xuemei.chen@ucr.edu
Website

Degree(s):

PhD 1995 Cornell University
BS 1988 Beijing University, China

College/Division Affiliation:

College of Natural and Agricultural Sciences

Center/Inst Affiliation(s):

Center for Plant Cell Biology

Areas Of Expertise:

Plant Development; Small Regulatory RNAs

Awards / Honors:

2007-2010  University Scholar, UC Riverside
2006  Charles Albert Shull award from American Society of Plant Biologists
2005  Board of Trustees Research Fellowship for Scholarly Excellence, Rutgers University
1995-1997  NIH Postdoctoral Fellowship
1991-1994  Cornell Plant Science Center Fellowship
1992  The Liu Memorial Award and The Hsien Wu and Daisy Yen Wu Scholarship

Research Summary:

The Arabidopsis flower is a great model to dissect developmental mechanisms underlying patterning. The flower comes from a group of undifferentiated cells known as the floral meristem. A series of cell fate specification events occurs within the floral meristem during flower development. The stem cells in the center of the floral meristem divide to produce daughter cells, some of which remain stem cells while others are displaced to the periphery of the meristem to become floral organ primordia. The floral meristem puts out four types of organ primordia successively in rings, or whorls. The first and second whorl primordia become sepals and petals, respectively, which are also known as perianth organs. The third and fourth whorl primordia become stamens and carpels, respectively, which are reproductive organs. Upon production of the carpel primordia, the stem cells in the floral meristem are terminated such that no more floral organs are generated. Therefore, floral patterning involves the temporal regulation of floral stem cells and the specification of floral organ identity among other patterning events.

 

 

Molecular genetic analyses by many labs led to the discovery of four classes of genes (the so-called A, B, C, and E genes) encoding transcription factors that act in combination to specify the four floral organ identities. While the class E genes act in all four whorls, the A, B, and C genes each acts in two adjacent whorls: A in whorls 1+2, B in whorls 2+3, and C in whorls 3+4. The unique composition of the ABCE genes in each whorl specifies the identity of the whorl: A+E for sepal, A+B+E for petal, B+C+E for stamen, and C+E for carpel. Another important genetic interaction is the antagonism between the A and C genes, which helps restrict them to their normal domains of activity. In the absence of A function, C function expands into the outer two whorls to convert perianth organs into reproductive organs. In the absence of C function, A function expands into the inner two whorls to convert reproductive organs into perianth organs. In addition to its role in specifying reproductive organ identities, the class C gene AGAMOUS (AG) also plays a key role in the timely termination of floral stem cells. In an ag loss-of-function mutant, floral stem cells continue to put out floral organs to result in a flowers-within-flower phenotype.

We have been interested in dissecting the AG pathway that specifies reproductive organ identities and regulates the termination of floral stem cells. As a postdoctoral fellow in Dr. Elliot Meyerowitz’s lab, I performed a sensitized genetic screen in the weak ag-4 mutant background to isolate mutations that further compromise the AG pathway. Mutations in two new genes, HUA1 and HUA2, enhance the ag-4 defect, suggesting that HUA1 and HUA2 play a role in the AG pathway. We took advantage of the weak phenotype of the hua1 hua2 double mutant and performed another genetic screen to isolate mutations that enhance the hua1 hua2 phenotype such that the flowers resemble ag mutant flowers. Mutations in five new genes, which we named HUAENHANCER (HEN)1-5, were isolated (Figure 1). The ag-like phenotypes of the hua1hua2 hen mutants suggest that the HEN genes all play a role in the AG pathway in flower development. We cloned the five HEN genes as well as HUA1 by map-based cloning.

Intriguingly, with the exception of HEN3 (Wang and Chen, 2004) [PDF], all HUA and HEN genes encode proteins with implicated cellular functions in RNA metabolism, suggesting that posttranscriptional mechanisms govern floral patterning. In particular, we found that HUA1, HUA2, HEN2, and HEN4 promote AG expression by preventing pre-mature transcription termination within the second intron of AG (Cheng et al., 2003) [PDF]. HEN1 encodes a novel protein required for the normal accumulation of microRNAs (Park et al., 2002) [PDF] and small interfering RNAs (siRNAs) (Boutet et al., 2003) [PDF]. Furthermore, we demonstrated that a microRNA, miR172, whose biogenesis requires HEN1, plays a key role as a repressor of the class A gene APETALA2 (AP2) (Chen, 2004) [PDF]. miR172 is specifically present in floral meristems (Figure 2 ). Mis-expression of MIR172 genes with the 35S promoter results in ap2 loss-of-function phenotypes (Figure 2 ). Mis-expression of AP2m3, a miR172-resistant version of AP2 cDNA but not wild-type AP2 cDNA, results in flowers that resemble ag loss-of-function mutants (Figure 2 ). Our current and future research involves the definition of the role of miR172 in flower development in relation to the AG-AP2 antagonistic pair and the further dissection of the mechanisms underlying the regulation of floral stem cells.

Selected Publications:

Lab Personnel: +

---

• Feedback
• Privacy Policy
• © 2007 Regents of the University of California