LEC1, FUS3, ABI3 and Em expression reveals no correlation with dormancy in Arabidopsis

Lars O Baumbusch, D Wayne Hughes, Glenn A Galau, Kjetill S Jakobsen
Journal of Experimental Botany 2004, 55 (394): 77-87
Dormant Arabidopsis seeds require stratification and light for germination. To study gene expression during establishment, maintenance and release of dormancy, various Arabidopsis ecotypes that are different in their degree of dormancy were investigated; three nsm mutants that lack the stratification-dependency, and the precocious germination and reduced dormancy of the abi3-1 mutant (insensitive to ABA). Genes examined by mRNA abundance include LEC1, FUS3 and ABI3, transcription factors that are major regulators of embryo development and, at least indirectly, play some role in the control of dormancy. Moreover, the late embryogenesis marker genes, AtEm1 and AtEm6, were examined in relation to the state of dormancy. The expression of LEC1, FUS3 and ABI3 mRNA is only marginally different during seed development in various strong or moderate dormancy wild types, nsm mutants and abi3-1. Therefore, it is unlikely that these transcription factors directly control the establishment of dormancy in Arabidopsis. Sole and various combina tions of light, temperature, and after-ripening regimes that alter germination behaviour were examined to determine if the expression of ABI3, AtEm1 and AtEm6 mRNAs were correlated with dormancy-breaking processes. ABI3 expression is influenced by cold and light, in a similar way in both dormant and non-dormant wild-type seeds. ABI3 transcript abundance in the nsm1 and nsm2 mutants is higher and in the nsm5-1 mutant is marginally lower than in wild-type seeds, but changes due to temperature and light factors are very similar to those that occur in wild-type seeds. The abundances of AtEm1 and AtEm6 mRNAs are equally affected by imbibition and cold temperature in mature and after-ripened seeds. The LEA transcript abundances for AtEm1 and AtEm6 are reduced in nsm mutants in a common, ABI3-independent pathway.

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