The embryonic leaf identity gene FUSCA3 regulates vegetative phase transitions by negatively modulating ethylene-regulated gene expression in Arabidopsis
- Equal contributors
1 Department of Cell and Systems Biology (CSB), University of Toronto, 25 Willcocks Street, Toronto, ON, M5S 3B2, Canada
2 Department of Biological Sciences, University of Toronto at Scarborough, 1265 Military Trail, Toronto, ON, M1C 1A4, Canada
3 Centre for the Analysis of Genome Evolution and Function (CAGEF), University of Toronto, 25 Harbord Street, Toronto, ON, M5S 3G5, Canada
BMC Biology 2012, 10:8 doi:10.1186/1741-7007-10-8Published: 20 February 2012
The embryonic temporal regulator FUSCA3 (FUS3) plays major roles in the establishment of embryonic leaf identity and the regulation of developmental timing. Loss-of-function mutations of this B3 domain transcription factor result in replacement of cotyledons with leaves and precocious germination, whereas constitutive misexpression causes the conversion of leaves into cotyledon-like organs and delays vegetative and reproductive phase transitions.
Herein we show that activation of FUS3 after germination dampens the expression of genes involved in the biosynthesis and response to the plant hormone ethylene, whereas a loss-of-function fus3 mutant shows many phenotypes consistent with increased ethylene signaling. This FUS3-dependent regulation of ethylene signaling also impinges on timing functions outside embryogenesis. Loss of FUS3 function results in accelerated vegetative phase change, and this is again partially dependent on functional ethylene signaling. This alteration in vegetative phase transition is dependent on both embryonic and vegetative FUS3 function, suggesting that this important transcriptional regulator controls both embryonic and vegetative developmental timing.
The results of this study indicate that the embryonic regulator FUS3 not only controls the embryonic-to-vegetative phase transition through hormonal (ABA/GA) regulation but also functions postembryonically to delay vegetative phase transitions by negatively modulating ethylene-regulated gene expression.