High impact information on dei

• In Egfr1F26 mutant embryos that lack functional Egfr expression, the levels of Delilah and beta1 tubulin are very low [1].
• Finally, activation of the Egfr signaling pathway by either ectopically secreted Spitz, or activated Ras, leads to the ectopic expression of Delilah [1].
• In loss-of-function vein mutant embryos, muscle-dependent differentiation of tendon cells, measured by the level of expression of specific markers (Delilah and beta1 tubulin) is blocked [1].
• This pattern was coincident with the known sites of attachment of the somatic muscles to tendon cells in the epidermis. delilah expression persists in snail mutant embryos which lack mesoderm, indicating that expression of the gene was not induced by attachment of the underlying muscles [2].
• We show that stv expression falls within known tendon and muscle cell transcriptional regulatory cascades, being downstream of stripe, but not of another tendon transcriptional regulator, delilah, and downstream of the muscle regulator, mef-2 [3].

Analytical, diagnostic and therapeutic context of dei

• In situ hybridization with the delilah cDNA localized the expression of the gene to a subset of cells in the epidermis which form a distinct pattern involving both the segmental boundaries and intrasegmental clusters [2].

References