Vegetative Phase Change in Maize: Biotic Resistance and Agronomic Performance

Chandler, M. A.; Riedeman, E. S.; Tracy, William F.

doi:10.1002/9780470880579.ch4

Cited by 1 publication

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“…In flowering plants, changes in the relative timing of juvenile and adult development can have major effects on traits such as leaf morphology and the onset of flowering (reviewed by Huijser and Schmid, 2011;Geuten and Coenen, 2013;Poethig, 2013). Resistance to herbivory, as well as changes in cell wall composition, also have an important temporal component (Abedon et al, 2006; reviewed by Boege andMarquis, 2005 andChandler et al, 2011). Thus, the study of developmental timing is crucial to our understanding of plant and animal ontogeny, physiology and evolution.…”

Section: Introductionmentioning

confidence: 99%

The Arabidopsis Mediator CDK8 module genes CCT (MED12) and GCT (MED13) are global regulators of developmental phase transitions

et al. 2014

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Temporal coordination of developmental programs is necessary for normal ontogeny, but the mechanism by which this is accomplished is still poorly understood. We have previously shown that two components of the Mediator CDK8 module encoded by CENTER CITY (CCT; Arabidopsis MED12) and GRAND CENTRAL (GCT; Arabidopsis MED13) are required for timing of pattern formation during embryogenesis. A morphological, molecular and genomic analysis of the post-embryonic phenotype of gct and cct mutants demonstrated that these genes also promote at least three subsequent developmental transitions: germination, vegetative phase change, and flowering. Genetic and molecular analyses indicate that GCT and CCT operate in parallel to gibberellic acid, a phytohormone known to regulate these same three transitions. We demonstrate that the delay in vegetative phase change in gct and cct is largely due to overexpression of miR156, and that the delay in flowering is due in part to upregulation of FLC. Thus, GCT and CCT coordinate vegetative and floral transitions by repressing the repressors miR156 and FLC. Our results suggest that MED12 and MED13 act as global regulators of developmental timing by fine-tuning the expression of temporal regulatory genes.

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