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Late Flowering (late + flowering)
Selected AbstractsMajor flowering time gene and polygene effects on chickpea seed weightPLANT BREEDING, Issue 6 2003R. Hovav Abstract The effect of the major flowering gene (PPD) on seed weight of chickpea was studied on 450 F3 families from reciprocal crosses between a small-seeded, early-flowering (PPD/PPD) type and a large-seeded, late flowering (PPD/PPD) cultivar. F4 progeny tests were carried out to determine the PPD genotypes of each individual F3. The effects of the PPD gene and the polygenes on mean seed weight were both significant. Genetic correlations between time to flowering and seed weight were positive and relatively high, suggesting that in certain genetic backgrounds it might be difficult to breed early-flowering cultivars without compromising seed weight. [source] Genome-wide analyses of the transcriptomes of salicylic acid-deficient versus wild-type plants uncover Pathogen and Circadian Controlled 1 (PCC1) as a regulator of flowering time in ArabidopsisPLANT CELL & ENVIRONMENT, Issue 1 2010SILVIA SEGARRA ABSTRACT Salicylic acid (SA) has been characterized as an activator of pathogen-triggered resistance of plants. SA also regulates developmental processes such as thermogenesis in floral organs and stress-induced flowering. To deepen our knowledge of the mechanism underlying SA regulation of flowering time in Arabidopsis, we compared the transcriptomes of SA-deficient late flowering genotypes with wild-type plants. Down- or up-regulated genes in SA-deficient plants were screened for responsiveness to ultraviolet (UV)-C light, which accelerates flowering in Arabidopsis. Among them, only Pathogen and Circadian Controlled 1 (PCC1) was up-regulated by UV-C light through a SA-dependent process. Moreover, UV-C light-activated expression of PCC1 was also dependent on the flowering activator CONSTANS (CO). PCC1 gene has a circadian-regulated developmental pattern of expression with low transcript levels after germination that increased abruptly by day 10. RNAi plants with very low expression of PCC1 gene were late flowering, defective in UV-C light acceleration of flowering and contained FLOWERING LOCUS T (FT) transcript levels below 5% of that detected in wild-type plants. Although PCC1 seems to function between CO and FT in the photoperiod-dependent flowering pathway, transgenic plants overexpressing a Glucocorticoid Receptor (GR)-fused version of CO strongly activated FT but not PCC1 after dexamethasone treatment. [source] Memories of winter: vernalization and the competence to flowerPLANT CELL & ENVIRONMENT, Issue 11 2000S. D. Michaels ABSTRACT The promotion of flowering in response to a prolonged exposure to cold temperatures (i.e. winter) is a useful adaptation for plant species that flower in the spring. This promotion is known as vernalization and results in a permanent memory of cold exposure. While the physiology of vernalization has been extensively studied in many species, the molecular mechanism of vernalization remains largely unknown. Recent studies, however, have revealed some of the molecular events that create the requirement for vernalization. In Arabidopsis, naturally occurring late-flowering ecotypes and plants containing late-flowering mutations in the autonomous floral-promotion pathway are relatively late flowering unless cold treated. The vernalization requirement of these late-flowering ecotypes and autonomous-pathway mutants is largely created by an upregulation of the floral inhibitor FLOWERING LOCUS C (FLC). After cold treatment, as imbibed seeds or young seedlings, FLC transcript levels are downregulated and remain low for the remainder of the plant's life, but return to high levels in the next generation. Plants containing a constitutively expressed 35S:FLC construct remain late flowering after cold treatment, indicating that FLC levels must be downregulated for vernalization to be effective. Thus the epigenetic downregulation of FLC appears to be a major target of the vernalization pathway and provides a molecular marker of the vernalized state. [source] The Arabidopsis TALE homeobox gene ATH1 controls floral competency through positive regulation of FLCTHE PLANT JOURNAL, Issue 5 2007Marcel Proveniers Summary Floral induction is controlled by a plethora of genes acting in different pathways that either repress or promote floral transition at the shoot apical meristem (SAM). During vegetative development high levels of floral repressors maintain the Arabidopsis SAM as incompetent to respond to promoting factors. Among these repressors, FLOWERING LOCUS C (FLC) is the most prominent. The processes underlying downregulation of FLC in response to environmental and developmental signals have been elucidated in considerable detail. However, the basal induction of FLC and its upregulation by FRIGIDA (FRI) are still poorly understood. Here we report the functional characterization of the ARABIDOPSIS THALIANA HOMEOBOX 1 (ATH1) gene. A function of ATH1 in floral repression is suggested by a gradual downregulation of ATH1 in the SAM prior to floral transition. Further evidence for such a function of ATH1 is provided by the vernalization-sensitive late flowering of plants that constitutively express ATH1. Analysis of lines that differ in FRI and/or FLC allele strength show that this late flowering is caused by upregulation of FLC as a result of synergism between ATH1 overexpression and FRI. Lack of ATH1, however, results in attenuated FLC levels independently of FRI, suggesting that ATH1 acts as a general activator of FLC expression. This is further corroborated by a reduction of FLC -mediated late flowering in fca-1 and fve-1 autonomous pathway backgrounds when combined with ath1. Since other floral repressors of the FLC clade are not significantly affected by ATH1, we conclude that ATH1 controls floral competency as a specific activator of FLC expression. [source] Lesions in the mRNA cap-binding gene ABA HYPERSENSITIVE 1 suppress FRIGIDA -mediated delayed flowering in ArabidopsisTHE PLANT JOURNAL, Issue 1 2004Isabel C. Bezerra Summary 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. [source] | ||||||||||