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The Plant Cell, Vol. 14, 547-558, March 2002, Copyright © 2002,
American Society of Plant Biologists

KNAT1 and ERECTA Regulate Inflorescence Architecture in Arabidopsis

Scott J. Douglasa, George Chuckb, Ronald E. Denglera, Lakshmi Pelecandaa and C. Daniel Riggs1,a

a Botany Department, University of Toronto, 1265 Military Trail, West Hill, Ontario M1C1A4, Canada
b Biology Department, University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093-0116

1 To whom correspondence should be addressed. E-mail riggs{at}utsc.utoronto.ca; fax 416-287-7642

Plant architecture is dictated by morphogenetic factors that specify the number and symmetry of lateral organs as well as their positions relative to the primary axis. Mutants defective in the patterning of leaves and floral organs have provided new insights on the signaling pathways involved, but there is comparatively little information regarding aspects of the patterning of stems, which play a dominant role in architecture. To this end, we have characterized five alleles of the brevipedicellus mutant of Arabidopsis, which exhibits reduced internode and pedicel lengths, bends at nodes, and downward-oriented flowers and siliques. Bends in stems correlate with a loss of chlorenchyma tissue at the node adjacent to lateral organs and in the abaxial regions of pedicels. A stripe of achlorophyllous tissue extends basipetally from each node and is positioned over the vasculature that services the corresponding lateral organ. Map-based cloning and complementation studies revealed that a null mutation in the KNAT1 homeobox gene is responsible for these pleiotropic phenotypes. Our observation that wild-type Arabidopsis plants also downregulate chlorenchyma development adjacent to lateral organs leads us to propose that KNAT1 and ERECTA are required to restrict the action of an asymmetrically localized, vasculature-associated chlorenchyma repressor at the nodes. Our data indicate that it is feasible to alter the architecture of ornamental and crop plants by manipulating these genetically defined pathways.




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