Open access publications in the SLU publication database

Abstract

Transition from a vegetative growth phase to flowering in plants occurs in response to both environmental conditions and endogenous signals. Identification of genes that are involved in regulating the time of flowering is of great importance in agri- and horticulture. Flowering-time genes can be used for crop improvement by, for instance, engineering plants to flower earlier. This shortening of the time to flowering could result in an extended growing season that could enable farmers to grow more than one crop each year. In this work, a gene knockout approach using T-DNA tagging and in vivo gene fusion has been employed to identify and characterise genes that are involved in regulating flowering time in the model plant Arabidopsis thaliana. This approach resulted in the identification of two genes, At4g20010 and its homologue At1g31010. Expression studies and GUS histochemical analysis of a reporter gene revealed that At4g20010 is mainly expressed in rapid growing tissues such as root tips, shoot apex, flowers and stem nodes. T-DNA insertional mutants of At4g20010 and At1g31010 exhibit a late-flowering phenotype that can largely be repressed by application of gibberellin. Plants with an insertional mutation in At4g20010 contain a reduced amount of the bioactive gibberellin GA4 compared to wild-type plants. The decreased level of GA4 is not due to a transcriptional repression of the GA-biosynthetic genes AtGA3ox1 or AtGA20ox1, since their expressions were increased in the mutant plants. In silico analyses revealed that the C-terminal protein sequences encoded by At4g20010 and At1g31010 contain RNA-binding motifs, whereas the N-terminal sequences have three-dimensional structures similar to single stranded nucleic acid-binding proteins. To conclude, At4g20010 and At1g31010 may encode two RNA-binding proteins that are involved in regulating flowering time in A. thaliana by affecting the metabolism of GA. This can be possible either by a positive regulation of GA3ox at the post-transcriptional level or by a negative regulation of GA2ox.