Control of flower development in Arabidopsis thaliana by APETALA1 and interacting genes
Abstract
Mutations in the APETALA1 gene disturb two phases of flower development, flower meristem specification and floral organ specification. These effects become manifest as a partial conversion of flowers into inflorescence shoots and a disruption of sepal and petal development. We describe the changes in an allelic series of nine apetala1 mutants and show that the two functions of APETALA1 are separable. We have also studied the interaction between APETALA1 and other floral genes by examining the phenotypes of multiply mutant plants and by in situ hybridization using probes for several floral control genes. The results suggest that the products of APETALA1 and another gene, LEAFY, are required to ensure that primordia arising on the flanks of the inflorescence apex adopt a floral fate, as opposed to becoming an inflorescence shoot. APETALA1 and LEAFY have distinct as well as overlapping functions and they appear to reinforce each other's action. CAULIFLOWER is a newly discovered gene which positively regulates both APETALA1 and LEAFY expression. All functions of CAULIFLOWER are redundant with those of APETALA1. APETALA2 also has an early function in reinforcing the action of APETALA1 and LEAFY, especially if the activity of either is compromised by mutation. After the identity of a flower primordium is specified, APETALA1 interacts with APETALA2 in controlling the development of the outer two whorls of floral organs.
Additional Information
Copyright © 1993 by Company of Biologists. (Accepted 26 July 1993) Special thanks go to Marty Yanofsky for making the AP1 probe available prior to publication and for constructive comments on the manuscript. We also thank Tom Jack, Gerd Bossinger, Megan Griffith and Alan Neale for helpful discussion of the manuscript. We are indebted to Maarten Koornneef and Luca Comai for supplying genetic material. Gunta Jaudzems provided excellent microscopy facilities. J.L.B. was supported by a Short Term Fellowship from the Human Frontiers Science Program and an Australian Research Council Postdoctoral Research Fellowship. J.A. held a Monash Postgraduate Scholarship. D.W. was supported by a EMBO Long Term Fellowship and a Senior Fellowship from the American Cancer Society, California Division. This work was supported by an Australian Research Council Grant A19131181 to D.R.S. and a US Department of Energy, Division of Energy Biosciences Grant DE-FG03-88ER13873 and a US National Science Foundation Grant MCB-9204839 to E.M.M.Attached Files
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Additional details
- Eprint ID
- 12447
- Resolver ID
- CaltechAUTHORS:BOWdev93
- Human Frontiers Science Program
- Australian Research Council
- A19131181
- Monash University
- European Molecular Biology Organization (EMBO)
- American Cancer Society, California Division
- Department of Energy
- DE-FG03-88ER13873
- National Science Foundation
- MCB-9204839
- Created
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2008-11-26Created from EPrint's datestamp field
- Updated
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2019-10-03Created from EPrint's last_modified field