The regulation of floral organ identity was investigated using a forward genetic approach in five floral homeotic mutants of
Floral development is one of the model systems for investigating the mechanisms underlying organogenesis in plants. Floral organ identity is controlled by the well-known ABC model, which has been generalized to many flowering plants. Here, we report a previously uncharacterized MYB-like gene,
- NSF-PAR ID:
- 10086257
- Publisher / Repository:
- Proceedings of the National Academy of Sciences
- Date Published:
- Journal Name:
- Proceedings of the National Academy of Sciences
- Volume:
- 116
- Issue:
- 11
- ISSN:
- 0027-8424
- Page Range / eLocation ID:
- p. 5176-5181
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
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Abstract Thalictrum , a noncore eudicot. We hypothesized that these mutants carry defects in the floral patterning genes. Mutant characterization comprised comparative floral morphology and organ identity gene expression at early and late developmental stages, followed by sequence analysis of coding and intronic regions to identify transcription factor binding sites and protein–protein interaction (PPI) motifs. Mutants exhibited altered expression of floral MADS‐box genes, which further informed the function of paralogs arising from gene duplications not found in reference model systems. The ensuing modified BCE models for the mutants supported instances of neofunctionalization (e.g., B‐class genes expressed ectopically in sepals), partial redundancy (E‐class), or subfunctionalization (C‐class) of paralogs. A lack of deleterious mutations in the coding regions of candidate floral MADS‐box genes suggested thatcis ‐regulatory ortrans ‐acting mutations are at play. Consistent with this hypothesis, double‐flower mutants had transposon insertions or showed signs of transposon activity in the regulatory intron ofAGAMOUS (AG ) orthologs. Single amino acid substitutions were also found, yet they did not fall on any of the identified DNA binding or PPI motifs. In conclusion, we present evidence suggesting that transposon activity and regulatory mutations in floral homeotic genes likely underlie the striking phenotypes of theseThalictrum floral homeotic mutants. -
Summary Many plants require prolonged exposure to cold to acquire the competence to flower. The process by which cold exposure results in competence is known as vernalization. In
Arabidopsis thaliana , vernalization leads to the stable repression of the floral repressor via chromatin modification, including an increase of trimethylation on lysine 27 of histone H3 (H3K27me3) by Polycomb Repressive Complex 2 (FLOWERING LOCUS CPRC 2). Vernalization in pooids is associated with the stable induction of a floral promoter, (VERNALIZATION 1VRN1 ). From a screen for mutants with a reduced vernalization requirement in the model grassBrachypodium distachyon , we identified two recessive alleles of (ENHANCER OF ZESTE ‐LIKE 1 ).EZL 1 is orthologous toEZL 1A. thaliana , a gene that encodes the catalytic subunit ofCURLY LEAF 1PRC 2.B. distachyon ezl1 mutants flower rapidly without vernalization in long‐day (LD ) photoperiods; thus, is required for the proper maintenance of the vegetative state prior to vernalization. Transcriptomic studies inEZL 1ezl1 revealed mis‐regulation of thousands of genes, including ectopic expression of several floral homeotic genes in leaves. Loss of results in the global reduction of H3K27me3 and H3K27me2, consistent with this gene making a major contribution toEZL 1PRC 2 activity inB. distachyon . Furthermore, inezl1 mutants, the flowering genes andVRN 1 (AGAMOUS ) are ectopically expressed and have reduced H3K27me3. Artificial microAG RNA knock‐down of either orVRN 1 inAG ezl1‐1 mutants partially restores wild‐type flowering behavior in non‐vernalized plants, suggesting that ectopic expression inezl1 mutants may contribute to the rapid‐flowering phenotype. -
Organ initiation from the shoot apical meristem first gives rise to leaves during vegetative development and then flowers during reproductive development.
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