Deletion of 153 bp of exon E4-intron I4 sequences of CRMP with an insertion of six nucleotides (Genbank GU452677). The predicted open reading frame created by the E4-I4 fusion terminates at an in-frame nonsense codon within intron I4, probably resulting in a severely truncated product consisting of only the N-terminal 10% of the CRMP protein.
5381 bp deletion associated with the imprecise excision of P{EP}CRMPEP3238, which removes the 3' end of exon 4 and the first nucleotide of intron 4 of CRMP.
CRMPsupK1 adults show circadian arrhythmicity. Their l-LNvs show a split POT.
Homozygous, hemizygous, or heteroallelic CRMPsupK1 mutants are viable, fertile, and morphologically normal when grown under standard laboratory conditions.
When tested for short term memory performance 2 minutes after a single aversive Pavlovian training session, CRMPsupK1/CRMPsupIa1 as well as homozygous CRMPsupK1 mutants exhibit significantly reduced performance compared with wild-type control flies. Medium-term memory performance measured 3 hours after a single aversive Pavlovian training session is also reduced in homozygous mutants and heteroallelic mutant animals.
Homozygous CRMPsupK1 mutants exhibit significantly reduced long-term memory performance compared with control animals.
Under free-running conditions (constant darkness), wild-type and CRMPsupK1 mutant animals exhibit similar overall activity. Period length is similar for all tested animals, indicating that the length of the circadian clock is not affected by CRMPsupK1. Compared with wild-type and heterozygous animals, significantly reduced arrhythmic power values indicating the relative strength of rhythmicity of free-running behaviours are observed among CRMPsupK1 homozygotes, CRMPsupK1/Df(3R)noi-B hemizygotes and CRMPsupK1/CRMPsupIa1 heteroallelic animals. Some individual CRMPsupK1 homozygotes and CRMPsupK1/Df(3R)noi-B hemizygotes lack significantly rhythmic behaviours (arrhythmic).
CRMPsupK1 is an enhancer of visible phenotype of Rac2EP3118, Scer\GAL4GMR.PF
CRMPsupK1 is a non-enhancer of visible phenotype of Rac1N17.UAS, Scer\GAL4sev.EP
CRMPsupK1 is a suppressor | partially of lethal | pharate adult stage phenotype of Scer\GAL4GMR.PF, sggUAS.cBa
CRMPsupK1 is a suppressor | partially of lethal | pharate adult stage phenotype of Scer\GAL4ey.PH, sggUAS.cBa
CRMPsupK1 is a suppressor | partially of visible | pharate adult stage phenotype of Scer\GAL4GMR.PF, sggUAS.cBa
CRMPsupK1 is a suppressor | partially of visible | pharate adult stage phenotype of Scer\GAL4ey.PH, sggUAS.cBa
CRMPsupK1 is a suppressor | partially of lethal | pupal stage phenotype of Scer\GAL4GMR.PF, sggUAS.cBa
CRMPsupK1 is a suppressor | partially of lethal | pupal stage phenotype of Scer\GAL4ey.PH, sggUAS.cBa
CRMPsupK1 is a non-suppressor of visible phenotype of Rac1N17.UAS, Scer\GAL4sev.EP
CRMPsupK1, Rac2EP3118, Scer\GAL4ey.PH has visible phenotype
CRMPsupK1, Rac1V12.UAS, Scer\GAL4sev.EP has visible phenotype
CRMPsupK1, Rac2EP3118, Scer\GAL4elav-C155 has visible phenotype
CRMPsupK1 is an enhancer of ommatidium phenotype of Rac2EP3118, Scer\GAL4GMR.PF
CRMPsupK1 is a non-enhancer of eye phenotype of Rac1N17.UAS, Scer\GAL4sev.EP
CRMPsupK1 is a suppressor | partially of eye | pharate adult stage phenotype of Scer\GAL4GMR.PF, sggUAS.cBa
CRMPsupK1 is a suppressor | partially of eye | pharate adult stage phenotype of Scer\GAL4ey.PH, sggUAS.cBa
CRMPsupK1 is a suppressor | partially of head | pharate adult stage phenotype of Scer\GAL4GMR.PF, sggUAS.cBa
CRMPsupK1 is a suppressor | partially of head | pharate adult stage phenotype of Scer\GAL4ey.PH, sggUAS.cBa
CRMPsupK1 is a non-suppressor of eye phenotype of Rac1N17.UAS, Scer\GAL4sev.EP
CRMPsupK1, Rac2EP3118, Scer\GAL4ey.PH has eye phenotype
CRMPsupK1, Rac1V12.UAS, Scer\GAL4sev.EP has eye phenotype
CRMPsupK1, Rac2EP3118, Scer\GAL4elav-C155 has eye phenotype
The rough eye phenotype resulting from the expression of Ras85DScer\UAS.cKa via Scer\GAL4GMR.PF is suppressed by homozygous CRMPsupK1.
CRMPsupK1 homozygotes expressing sggScer\UAS.cBa under the control of either Scer\GAL4GMR.PF or Scer\GAL4ey.PH regularly survive to the pharate adult stage and frequently eclose as adults displaying reduced rough eyes.
Severely reduced eyes are produced in homozygous CRMPsupK1 animals also expressing Rac1V12.Scer\UAS under the control of Scer\GAL4sev.EP.
Animals expressing dominant-negative Rac1N17.Scer\UAS under the control of Scer\GAL4sev.EP display no discernible differences in the presence or absence of homozygous CRMPsupK1.
The eye phenotype resulting from the expression of Rac2EP3118 under the control of Scer\GAL4GMR.PF is enhanced in CRMPsupK1 animals that have reduced eyes with extensively fused ommatidia.
The Scer\GAL4ey.PH driver produces irregular ommatidial arrangements and reduced eyes in Rac2EP3118 animals that are homozygous for CRMPsupK1.
Pan-neural expression of Rac2EP3118 with Scer\GAL4elav-C155 in CRMPsupK1 homozygotes results in rough eyes.
CRMPT:Avic\GFP-EGFP supports the suppression of the body colour phenotype of bunspecified, CRMPsupK1 double mutants by rSu(b).cSa resulting in a brownish cuticle.
CRMPfs9a.T:Avic\GFP-EGFP fails to support the suppression of the body colour phenotype of bunspecified, CRMPsupA4/CRMPsupK1 double mutants by rSu(b).cSa resulting in a dark gray cuticle.
CRMPfs9b.T:Avic\GFP-EGFP supports the suppression of the body colour phenotype of bunspecified, CRMPsupA4/CRMPsupK1 double mutants by rSu(b).cSa resulting in a brownish cuticle.