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First published online 13 August 2008
doi: 10.1242/dev.024273


Development 135, 3013-3019 (2008)
Published by The Company of Biologists 2008


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Research Report

Floral meristem initiation and meristem cell fate are regulated by the maize AP2 genes ids1 and sid1

George Chuck1,*, Robert Meeley2 and Sarah Hake1

1 Plant Gene Expression Center, United States Department of Agriculture - Agriculture Research Service and the University of California, Albany, CA 94710, USA.
2 Pioneer - A DuPont Company, Johnston, IA 50131, USA.

* Author for correspondence (e-mail: gchuck{at}nature.berkeley.edu)

Accepted 9 July 2008

SUMMARY

Grass flowers are organized on small branches known as spikelets. In maize, the spikelet meristem is determinate, producing one floral meristem and then converting into a second floral meristem. The APETALA2 (AP2)-like gene indeterminate spikelet1 (ids1) is required for the timely conversion of the spikelet meristem into the floral meristem. Ectopic expression of ids1 in the tassel, resulting from a failure of regulation by the tasselseed4 microRNA, causes feminization and the formation of extra floral meristems. Here we show that ids1 and the related gene, sister of indeterminate spikelet1 (sid1), play multiple roles in inflorescence architecture in maize. Both genes are needed for branching of the inflorescence meristem, to initiate floral meristems and to control spikelet meristem determinacy. We show that reducing the levels of ids1 and sid1 fully suppresses the tasselseed4 phenotype, suggesting that these genes are major targets of this microRNA. Finally, sid1 and ids1 repress AGAMOUS-like MADS-box transcription factors within the lateral organs of the spikelet, similar to the function of AP2 in Arabidopsis, where it is required for floral organ fate. Thus, although the targets of the AP2 genes are conserved between maize and Arabidopsis, the genes themselves have adopted novel meristem functions in monocots.

Key words: AP2, Maize, Meristem, miR172


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A-maize-ing meristem regulation

Development 2008 135: e1802. [Full Text]  






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