Construct: Ras85DV12 coding region expression is driven by a heat shock promoter.
This somatic variant has been found associated with cancer in each of the three paralogous genes in human (KRAS, HRAS, NRAS).
Ras85DV12.hs heterozygous flies maintained at 25[o]C exhibit normal life spans and locomotor activity.
Overexpression of Ras85DV12.hs does not affect superoxide production.
Expression of Ras85DV12.hs using heat shock at 24 hours after puparium formation results in extra lattice cells in the retina; there are an average of 18.5 +/- 0.3 cells per ommatidial unit (compared to 12 cells per ommatidial unit in wild-type animals).
Heat shock expression of Ras85DV12.hs can lead to a morphogenetic furrow arrest phenotype in the developing eye.
Expression of Ras85DV12.hs during late larval development using heat shock results in flies that show a loss of wing veins.
Ablation of cone cells in four adjacent developing ommatidia at 20 hrs APF causes death of interommatidial precursor cells in wild type. This IPC death is blocked by Nfa-g62 or Ras85DV12.hs.
Transient expression by heat shock during early pupal development (0-5.5 hr APF) causes an increase in cone-like cells. Heat shock during later pupal development (20-40 hr APF) has no effect on cone cells but causes an increase in the number of secondary and tertiary pigment cells.
Ras85DV12.hs has ommatidium phenotype, enhanceable by klu[+]/kluunspecified
Ras85DV12.hs is a suppressor of cone cell phenotype of aosGMR.PS
kluunspecified/+ enhances the extra cell phenotype seen in the retina of animals expressing Ras85DV12.hs using heat shock at 24 hours after puparium formation; the double mutant animals have an average of 20.03 +/- 0.2 cells per ommatidial unit (compared to an average of 18.5 +/- 0.3 cells per ommatidial unit in animals expressing Ras85DV12.hs at the same time in a klu+ background).
Flies carrying both Ras85DV12.hs and argosGMR.PS show a normal number of cone cells in most ommatidia.
N. Perrimon