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FB2026_01
,
released March 12, 2026
[92A5-92A5];[92A11-92A11];
A set of isogenic deficiency stocks created by FLP-induced recombination between FRT-carrying transgenic insertions; molecularly defined deletion endpoints correspond to initial location of the progenitor insertions. Initial set of 519 isogenic deletions provides 56% genome coverage.
The current Exelixis collection at the Bloomington Stock Center differs from the original described in FBrf0175003 : a significant number were shown not to carry a deletion and have been removed from the collection; a number of stocks have been lost; a number of additional deletions are included that were generated after publication.
92A5;92A11
Breakpoint based on release 3 sequence coordinate from Parks et al., 2004 (FBrf0174230), converted to release 5 coordinate.
Df(3R)Exel6184/Df(3R)Delta-X43 flies show defects in cardiac function at both 1 and 5 weeks of age (systolic diameter is increased and fractional shortening is decreased compared to wild type).
Df(3R)Delta-X43/Df(3R)Exel6184 flies (in which most Dys isoforms are absent) have a significantly shorter lifespan than wild-type controls, while single heterozygotes show a moderate lifespan reduction.
Df(3R)Delta-X43/Df(3R)Exel6184 flies develop age-dependent abnormalities in the heart muscle throughout adult life, with increasingly disorganized myocardial myofibrils and gaps. With age, flies exhibit shorter diastolic intervals, resulting in increased heart rates and fewer asystoles, and produce a more regular heartbeat than wild-type controls.
Expressing Mmus\DmdDp116.UAS under the control of Scer\GAL4how-24B rescues the increased systolic diameter and reduced fractional shortening of the heart wall in Df(3R)Delta-X43/Df(3R)Exel6184 adult flies.
Throughout their adult life, Df(3R)Delta-X43/Df(3R)Exel6184 flies have a significantly wider diastolic and systolic diameter, accompanied by a reduced fractional shortening compared to controls, while single heterozygotes show increased diameter phenotypes without a reduction in fractional shortening.
Overall activity of Df(3R)Exel6184 mutant flies is reduced compared to controls.
No obvious defects in muscle morphology are seen in Df(3R)Exel6184/+ mutant flies.
Increased muscle degeneration is seen in homozygous Df(3R)Exel6184 mutant flies at 25[o]C and, as in wild type, the phenotype is increased ~2 fold by an increase in temperature to 33[o]C. On paraquat-containing food the ratio or degree of muscle degeneration is not increased in Df(3R)Exel6184 mutant flies in comparison to control. Unlike in wild type, animals exposure of Df(3R)Exel6184 mutants to lower temperature (18[o]C) causes the appearance of severe progressive degeneration, followed by focal muscle loss. At 25[o]C the phenotype becomes more severe with age. Sugar-free food conditions do not promote severe muscle loss. Metabolic rate on sugar-free food is reduced compared to wild type controls.
Df(3R)Exel6184 mutant flies exhibit temperature-induced mobility defects.
Df(3R)Exel6184 homozygotes display a significant increase in the frequency of lamina plexus defects in the brain of third instar larvae as well as reduced rhabdomere length in the adult eye.
Homozygous viable.
Eggs laid by homozygous females are shorter and rounder than wild type.
Homozygotes show a posterior crossvein phenotype. 71% of wings have a "detached" phenotype (the crossvein is detached from both L4 and L5), and wings with a "gapped" phenotype (the crossvein is detached from either vein L4 or L5, but not both) and "point" phenotype (the crossvein is reduced to a point) are also seen.
Heterozygotes have a normal wing vein pattern.
Voltage-clamp recordings from either the aCC or RP2 motor neurons reveals that synaptic currents are significantly increased in amplitude in Df(3R)Exel6184 heterozygotes.
Df(3R)Exel6184 flies exhibit significant systolic impairment and dilated end diastolic dimensions compared to controls.