†Present address: EMBRAPA Hortaliças, Centro Nacional de Pesquisa de Hortaliças, CP 218 70359-970 Brasilia - DF - Brazil.
Lesions in the mRNA cap-binding gene ABA HYPERSENSITIVE 1 suppress FRIGIDA-mediated delayed flowering in Arabidopsis
Article first published online: 11 AUG 2004
The Plant Journal
Volume 40, Issue 1, pages 112–119, October 2004
How to Cite
Bezerra, I. C., Michaels, S. D., Schomburg, F. M. and Amasino, R. M. (2004), Lesions in the mRNA cap-binding gene ABA HYPERSENSITIVE 1 suppress FRIGIDA-mediated delayed flowering in Arabidopsis. The Plant Journal, 40: 112–119. doi: 10.1111/j.1365-313X.2004.02194.x
- Issue published online: 11 AUG 2004
- Article first published online: 11 AUG 2004
- Received 14 April 2004; revised 4 June 2004; accepted 5 July 2004.
- leaf development;
- abscisic acid;
- winter annual;
Recessive mutations that suppress the late-flowering phenotype conferred by FRIGIDA (FRI) and FLOWERING LOCUS C (FLC) and which also result in serrated leaf morphology were identified in T-DNA and fast-neutron mutant populations. Molecular analysis showed that the mutations are caused by lesions in the gene encoding the large subunit of the nuclear mRNA cap-binding protein, ABH1 (ABA hypersensitive1). The suppression of late flowering is caused by the inability of FRI to increase FLC mRNA levels in the abh1 mutant background. The serrated leaf morphology of abh1 is similar to the serrate (se) mutant and, like abh1, se is also a suppressor of FRI-mediated late flowering although it is a weaker suppressor than abh1. Unlike se, in abh1 the rate of leaf production and the number of juvenile leaves are not altered. The abh1 lesion affects several developmental processes, perhaps because the processing of certain mRNAs in these pathways is more sensitive to loss of cap-binding activity than the majority of cellular mRNAs.