Molecular Plant Advance Access originally published online on June 3, 2008
Molecular Plant 2008 1(4):645-658; doi:10.1093/mp/ssn029
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Regulation of Arabidopsis Early Anther Development by the Mitogen-Activated Protein Kinases, MPK3 and MPK6, and the ERECTA and Related Receptor-Like Kinases
a Department of Biology and the Huck Institutes of the Life Sciences, Pennsylvania State University, University Park, PA 16802, USA
b The Intercollege Graduate Program in Plant Biology, Pennsylvania State University, University Park, PA 16802 USA
c Present address: 3015 Quinby Dr., Columbus, OH 43232, USA
d Present address: 318 Coker Hall (CB# 3280), Department of Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-3280, USA
e Department of Biology, University of Washington, Seattle, WA 98195, USA
f Present address: Monsanto Company, 700 Chesterfield Pkwy North, Mailzone GG4G, Chesterfield, MO 63017, USA
g Department of Biochemistry and Bond Life Sciences Center, University of Missouri, Columbia, MO 65211, USA
1 To whom correspondence should be addressed. E-mail hxm16{at}psu.edu, fax 814-863-1357.
Mitogen-activated protein kinase (MAPK) and leucine-rich repeat receptor-like kinase (LRR-RLK) signaling pathways have been shown to regulate diverse aspects of plant growth and development. In Arabidopsis, proper anther development relies on intercellular communication to coordinate cell proliferation and differentiation. Two closely related genes encoding MAPKs, MPK3 and MPK6, function redundantly in regulating stomatal patterning. Although the mpk6 mutant has reduced fertility, the function of MPK3 and MPK6 in anther development has not been characterized. Similarly, the ERECTA (ER), ERECTA-LIKE1 (ERL1) and ERL2 genes encoding LRR-RLKs function together to direct stomatal cell fate specification and the er-105 erl1-2 erl2-1 triple mutant is sterile. Because the mpk3 mpk6 double null mutant is embryo lethal, anther development was characterized in the viable mpk3/+ mpk6/– and er-105 erl1-2 erl2-1 mutants. We found that both mutant anthers usually fail to form one or more of the four anther lobes, with the er-105 erl1-2 erl2-1 triple mutant exhibiting more severe phenotypes than those of the mpk3/+ mpk6/– mutant. The somatic cell layers of the differentiated mutant lobes appeared larger and more disorganized than that of wild-type. In addition, the er-105 erl1-2 erl2-1 triple mutant has a reduced number of stamens, the majority of which possess completely undifferentiated or under-differentiated anthers. Furthermore, sometimes, the mpk3/+ mpk6/– mutant anthers do not dehisce, and the er-105 erl1-2 erl2-1 anthers were not observed to dehisce. Therefore, our results indicate that both ER/ERL1/ERL2 and MPK3/MPK6 play important roles in normal anther lobe formation and anther cell differentiation. The close functional relationship between these genes in other developmental processes and the similarities in anther developmental phenotypes of the two types of mutants reported here further suggest the possibility that these genes might also function in the same pathway to regulate anther cell division and differentiation.