Temperature-Sensitive Splicing in the Floral Homeotic Mutant apetala3-1
Abstract
The floral homeotic gene APETALA3 (AP3) is required for stamen and petal development in Arabidopsis. The previously described ap3-1 allele is temperature sensitive and carries a missense mutation near a 5′ splice site. The missense mutation lies within a domain of the AP3 protein that is thought to be important for protein–protein interactions, which suggests that temperature sensitivity of ap3-1 could reflect an unstable interaction with cofactors. Here, we show instead that the ap3-1 mutation causes a temperature-dependent splicing defect and that temperature sensitivity is not a property of the protein products of ap3-1 but of RNA processing, possibly because of unstable base pairing between the transcript and small nuclear RNAs. The unexpected defect of the ap3-1 mutant offers unique opportunities for genetic and molecular studies of splice site recognition in plants.
Additional Information
© 1998 American Society of Plant Physiologists. Received April 20, 1998; accepted July 13, 1998. Published September 1, 1998. We are grateful to Dr. Tom Jack for the pF733 plasmid and anti-AP3 antiserum and for communicating results before publication and to Drs. Gordon Simpson, Tracy Johnson, John Wagner, Tom Jack, Jennifer Fletcher, Prakash Kumar, Steve Jacobsen, Eva Ziegelhoffer, Carolyn Ohno, and Chiou-Fen Chuang for critical reading of the manuscript. R.W.M.S. was supported by a long-term fellowship (No. LT-12/95) from the Human Frontier Science Program, and work in E.M.M.'s laboratory is supported by a grant from the National Science Foundation (No. MCB-9603821).Additional details
- PMCID
- PMC144071
- Eprint ID
- 72820
- Resolver ID
- CaltechAUTHORS:20161214-121625447
- LT-12/95
- Human Frontier Science Program
- MCB-9603821
- NSF
- Created
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2016-12-14Created from EPrint's datestamp field
- Updated
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2021-11-11Created from EPrint's last_modified field