The DOI matches its Crossref record; 45 of the 45 references it cites were found in a registry or an index.
Disruption of an RNA helicase/RNAse III gene in Arabidopsis causes unregulated cell division in floral meristems
Abstract
Arabidopsis thaliana floral meristems are determinate structures that produce a defined number of organs, after which cell division ceases. A new recessive mutant, carpel factory (caf), converts the floral meristems to an indeterminate state. They produce extra whorls of stamens, and an indefinite number of carpels. Thus, CAF appears to suppress cell division in floral meristems. The function of CAF is partially redundant with the function of the CLAVATA (CLV) and SUPERMAN (SUP) genes, as caf clv and caf sup double mutants show dramatically enhanced floral meristem over-proliferation. caf mutant plants also show other defects, including absence of axillary inflorescence meristems, and abnormally shaped leaves and floral organs. The CAF gene was cloned and found to encode a putative protein of 1909 amino acids containing an N-terminal DExH/DEAD-box type RNA helicase domain attached to a C-terminal RNaseIII-like domain. A very similar protein of unknown function is encoded by a fungal and an animal genome. Helicase proteins are involved in a number of processes, including specific mRNA localization and mRNA splicing. RNase III proteins are involved in the processing of rRNA and some mRNA molecules. Thus CAF may act through some type of RNA processing event(s). CAF gives rise to two major transcripts of 2.5 and 6.2 kb. In situ hybridization experiments show that CAF RNA is expressed throughout all shoot tissues.
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Metadata
- Authors
- Jacobsen, S. E., Running, M. P., & Meyerowitz, E. M.
- Venue
- Development
- Publisher
- The Company of Biologists
- Published
- 1999-12-01
- Volume
- 126
- Issue
- 23
- Pages
- 5231-5243
- ISSN
- 0950-1991 (ISSN-L)
- 1477-9129
- OpenAlex
- W2168106981
- Cited by
- 371
- References
- 45
- FWCI
- 40.05
- Type
- journal article
- Language
- en
- Open access
- closed
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