An Hsp70 promoter drives expression of the Raf coding sequence in which amino acid residues 2-431 have been deleted.
Expression of phlF22.hs during the late third larval instar stage using heat shock results in flies that show a significant amount of wing vein loss. Heat shock during the early-to-mid second larval instar stages results in flies with ectopic wing vein tissue, in most cases in close proximity to a vein.
Ubiquitous expression in the embryo weakly suppresses normal cell death.
Modulation of voltage gated K+ currents induced by the neuropeptide pituitary adenylyl cyclase-activating polypeptide (PACAP38) is eliminated. The mutation fails to block or mimic PACAP38 (neuropeptide pituitary adenylyl cyclase-activating polypeptide) induced enhancement of K+ currents.
After 3 days of heat shock homozygous females lay dorsalised embryos, dorsal appendages are fused in a ring at the anterior end and eggs are smaller and more spherical than wild type (comparable to eggs laid by fs(1)K101 females). Some embryos exhibit a more severe phenotype. Expression of Hsap\RAF1gof.hs leads to more embryos exhibiting the stronger chorion phenotype.
Females lay eggs with a dorsalised chorion.
RafF22.hs is a non-suppressor of abnormal locomotor rhythm phenotype of Nf1P1
RafF22.hs has dorsal appendage phenotype, enhanceable by dodhs.PH
RafF22.hs has egg chorion phenotype, suppressible by Dsor1+t9
A.H. Brand and N. Perrimon.
Constitutively active form of phl.