BACKGROUND: Mitogen-activated protein kinase (MAPK) cascades (p38, JNK, ERK 
pathways) are involved in cell fate acquisition during development. These kinase 
modules are associated with scaffold proteins that control their activity. In 
Drosophila, dMP1, that encodes an ERK scaffold protein, regulates ERK signaling 
during wing development and contributes to intervein and vein cell 
differentiation. Functional relationships during wing development between a 
chromatin regulator, the Enhancer of Trithorax and Polycomb Corto, ERK and its 
scaffold protein dMP1, are examined here.
RESULTS: Genetic interactions show that corto and dMP1 act together to 
antagonize rolled (which encodes ERK) in the future intervein cells, thus 
promoting intervein fate. Although Corto, ERK and dMP1 are present in both 
cytoplasmic and nucleus compartments, they interact exclusively in nucleus 
extracts. Furthermore, Corto, ERK and dMP1 co-localize on several sites on 
polytene chromosomes, suggesting that they regulate gene expression directly on 
chromatin. Finally, Corto is phosphorylated. Interestingly, its phosphorylation 
pattern differs between cytoplasm and nucleus and changes upon ERK activation.
CONCLUSIONS: Our data therefore suggest that the Enhancer of Trithorax and 
Polycomb Corto could participate in regulating vein and intervein genes during 
wing tissue development in response to ERK signaling.