|Feature type||allele||Associated gene||Dmel\rl|
|Allele class||loss of function allele, hypomorphic allele - genetic evidence|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
|Carried on aberration|
|Phenotype Manifest In|
Homozygotes have a mild rough eye phenotype and show loss of wing vein material.
Evoked excitatory junction potentials at neuromuscular junctions are decreased in rl homozygous larvae.
Homozygotes have a rough eye phenotype, with fewer rhabdomeres per ommatidium (6.04 +/- 1.09) compared to wild type (6.99 +/- 0.07). The number of cone cells is reduced at the pupal stage compared to wild type and the development of the eye is disordered at the third larval instar.
Homozygotes often have gaps in wing vein 4.
Homozygotes have rolled and frayed wing blades.
Wing vein L4 is thinned or disrupted distal to the posterior crossvein.
Approximately 88% of rl1/Df(2R)PRF hemizygotes eclose compared to their heterozygous siblings at 18oC. Surviving adults have reduced eyes, rolled wings which may be blistered and defects in wing veins L3, L4 and L5.
The extra wing vein and eye phenotypes of rlSu23/+ flies are significantly enhanced by rl1. rlSu14/rl1 flies occasionally have extra wing vein material.
rl1 in transheterozygous combination with rl41-1, rlA3-2, rl21-1, rlZ3, rlZ7 or rl19 produces flies with rough eyes and bent wings.
Mild impact on R7 formation: 22% of ommatidia lack R7 cells. Double mutants with sl1 or sl2 show phenotypes very close to that of rl1 alone.
Hypersensitivity to oxidative stress (paraquat) and ionising radiation.
rl1 hemizygotes have rough eyes and bent down wings. Sections through the eye reveal a lack of most R7 cells and a reduced number of outer photoreceptor cells. A central portion of the L4 wing vein is missing.
rl1/Df(2R)rl10a strongly enhances the wing phenotype of Egfrt1/Egfrf37, N55e11/+ and vvlM3, and of alleles of ast, rho, vn, Vno, tt, and Abruptex alleles of N. rl1/Df(2R)rl10a suppresses the wing phenotype of EgfrE3 and of alleles of Ras64B, ci, net and px.
viable, RK2. wing edges rolled downward; margins somewhat frayed; L4 interrupted distal to posterior crossvein. Eyes small, dark and rough. Most extreme at 26oC, less extreme above and below that temperature (Lakovaara, 1963). Temperature sensitive period for eye phenotype during larval stages with most sensitive stage about 60 hr after hatching, i.e., at the beginning of the third instar (Hackman and Lakovaara, 1966). Effects of dosage of rl and rl+ on eye pigment deposition investigated by Lakovaara (1966).
|NOT Enhancer of|
rl[+], rl1, phl[+], phl12 is a suppressor | partially of small body | pupal stage phenotype of Nf1E2
|NOT Suppressor of|
|Phenotype Manifest In|
|NOT suppressed by|
|NOT Enhancer of|
rl[+]/rl1 is a suppressor of eye photoreceptor cell | ectopic phenotype of PDZ-GEFEP388, Scer\GAL4GMR.PF/Scer\GAL4GMR.PF
|NOT Suppressor of|
One copy of rl partially suppresses the percentage of sl mutant ommatidia that contain extra R7 photoreceptors.
The extra wing vein phenotype seen in Egfr[E1]/+ flies is dominantly suppressed by rl. The loss of wing veins and rough eye phenotype seen in rl homozygotes is dominantly enhanced by mago and by mago.
The structural defects seen in the neuromuscular junctions (NMJ) of Atg1 homozygous larvae are almost completely suppressed by rl/rl: synaptic density and apposition of pre and post synaptic components are restored and NMJ size is partially restored. Despite the fact that evoked excitatory junction potentials at larval NMJs are decreased in both rl homozygous and Atg1 homozygous larvae, this phenotype is not see in rl Atg1 double homozygotes. The accumulation of synaptic material in the axons of of motor neurons in Atg1 homozygous larvae is not suppressed by rl/rl.
The rough eye phenotype, irregular ommatidial array and increased photoreceptor cell number caused by expression of Gef26EP388 under the control of Scer\GAL4GMR.PF are strongly suppressed by rl1/+.
The rate of eclosion of rl1/Df(2R)PRF flies at 18oC is nearly halved by the presence of Su(var)205205. The eye and wing defects of surviving adults are enhanced.
rl1 recessively enhances the eye and wing defects associated with the asp1/aspDD3 mutant. The brain neuroblast mitotic index of double mutants with asp1 is generally as for asp1 mutants alone. The rl1; asp1 double mutant also displays an increase in the number of mitotic figures that show lagging chromatids at anaphase, and a low frequency of abnormal mitotic figures where the telomeric ends of chromosomes appear to remain in contact, forming daisy chains. The frequency of aneuploid and polyploid figures is significantly increased compared to asp1 single mutants.
Egfrt1 enhances the bristle, ocellar, wing and limb phenotypes of homozygotes. Bristle hyperplasia, ocellus enlargement and ocellus fusion are enhanced. Wings are notched, wing margins are hairier and have ectopic vein material. Legs are fused and bifurcated.
|Complementation & Rescue Data|
|Partially rescued by|
rl1 is partially rescued by rlhs.T:SV40\nls2,T:Scer\GAL4,T:Hsim\VP16,T:Hsim\gD
|Stocks ( 6 )|
|Notes on Origin|
Bridges, 23rd June 1922.
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 1 )|
|Secondary FlyBase IDs|
|References ( 29 )|
|Generate a list of|
|List References by type|
|Recent research papers ( 1 )|