phlF22.hs heterozygous flies maintained at 25[o]C exhibit normal life spans and locomotor activity.
Overexpression of phlF22.hs does not affect superoxide production.
16.6% of eggs derived from females expressing one copy of phlF22.hs using heat shock are dorsalised, with dorsal appendage material being expanded throughout the anterior of the egg. The penetrance of the dorsalised egg phenotype is 61.7% if the females express two copies of phlF22.hs.
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.
Expression of an activated phl mutation has no effect on size of Nf1 mutant pupae.
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.