Table 1.
Drosophila mutants named in Section 7. UAS—upstream activating sequence; UCP—uncoupled protein; HTT—huntingtin; CAG—cytosine–adenine–guanine; HD—Huntington’s disease; * Referenced in text as.
| · Allele Symbol (* Referenced in text as) |
Alternative Names | FlyBase ID | General Description |
|---|---|---|---|
| · Hsap\HTT200Q.UAS * FL-HTTQ200 |
Hsap\HTT200Q.Scer\UAS
HsapHTT200Q.UAS |
FBal0323497 | UAS regulatory sequences drive the expression of a full-length Hsap\HTT, containing an expanded 200 polyQ repeat. Induces rapid age-progressive decline of locomotor abilities in adult flies. Progressive defects of locomotor behavior. |
| · Hsap\HTTQ128.Scer\UAS * pUAS-Htt128Q |
UAS-Htt-Q128, Htt-Q128, UAS-HttQ128, UAS-Htt548aa-128Q, Hsap\HDQ128.Scer\UAS, Hsap\HTTQ128.Scer\UAs, HttQ128 | FBal0156385 | Scer\UAS sequences drive expression of the N-terminal 548 aa of the Q128 Hsap\HD cDNA, which encodes the pathogenic protein. Defective for behavior, circadian rhythm, eye color, locomotor behavior, and neuroanatomy. Reduced photoreceptor depolarization and complete abolishment of synaptic transmission in response to light. Cytoplasmic Hsap\HD aggregates are seen in neurons and non-neural tissues, aggregates are transported in larval motor axons, and accumulate in presynaptic neuromuscular junction terminals. Uncoordinated movement and abnormal grooming behavior. Premature death. |
| · Hsap\HTTQ93.ex1.Scer\UAS * Httex1pQ93 * UASHTT-EX1-PQ93/CyO * UAS-Htt exon1-Q93 * Htt93Q |
UAS-Httex1p Q93, Httex1p Q93, UAS-htt exon-1-Q93, UAS-Httex1p-Q93, P{UAS-Httex1p Q93}, Htt93Q, Httex1-93Q, UASHTT-EX1-PQ93, HttEx1Q93, P{UAS-Httex1p Q93}4F1 | FBal0127292 | Leads to an obvious loss of one or more photoreceptors, leading to a disorganization of ommatidia, exhibiting a progressive loss of vision. Results in the formation of aggregates in larval eye imaginal discs and subsequent age-dependent retinal degeneration and visual impairment. Neural degeneration and alteration of the diameter of synaptic vesicles, accumulation of organelles is seen in neurons producing a defect in axonal transport, increasing cell death. Initially hyperactive with gradual loss. Reduces mobility and lifespan. |
| · HsapHTTQ138.Scer\UAS.T:Disc\RFP-mRFP * UAS-mRFP.Htt.138Q |
Hsap\HTTQ138.Scer\UAS.T:Disc\RFP-mRFP | FBal0267405 | Containing a pathogenic tract of 138 polyQ repeats. Defects on grooming behavior, locomotor behavior, neuroanatomy, and increased cell death in the central brain and optic lobes. Neurons display morphological indicators of reduced neuronal health, including smaller neuromeres, increased branching, and reduced axonal connectivity. Premature death. |
| · UAS-mRFP.Htt.15Q * UAS-mRFP.Htt.15Q |
Hsap\HTTQ15.Scer\UAS.T:Disc\RFP-mRFP | Control for UAS-mRFP.Htt.138Q | Non-expanded human HTT control. |
| · GMR-GAL4UAS-127Q * GMR-GAL4UAS-127Q |
Zzzz\CAG127Q.Scer\UAS.T:Ivir\HA1 | Information in the literature [102] | Containing the expanded 127-CAG repeat. Severe abnormal eyes. |
| · Hsap\HTTGMR.Q120 * gmr-Htt(exon1)Q120 |
gmr-HttQ120 gmr-Htt-Q120 gmr-Q120 Q120 gmrHtt(exon1)Q120 GMR-HD.Q120 GMR-HTT.Q120 Between others |
FBtp0010067 | Expression of Hsap\HD amino acids 1–170, with 120 CAG glutamine repeats is governed by the glass multiple reporter (GMR) promoter. Results in neurodegeneration and the loss of rhabdomeres. Show a progressive decrease in the number of visible rhabdomeres per ommatidium. The eyes of flies expressing this allele progressively degenerate. |
| · Dmel\Rab5Scer\UAS.T:Avic\GFP-EGFP * CyO/If; UAS-Rab5-EGFP-elavGal4/MKRS |
UAS-GFP-Rab5
Rab5-GFP UAS-Rab5-GFP GFP-Rab5 UAS-GFPRab5 UASrab5-GFP UAS-GFP:Rab5 |
FBal0182041 | Modeled by Hsap\HTTGMR.Q120. Flies expressing this allele show trichome polarity defects in the wings, and alterations in the synaptic area under the regulation of Scer\GAL4 does not significantly alter the synaptic area. |
| · Dmel\HsfdsRNA.Scer\UAS * UAS-HSF1-RNAi |
HSF1 RNAi
UAS-Hsf.RNAi UAS-HSF1-RNAi HsfdsRNA.Scer\UAS |
FBal0283110 | Defects on neuroanatomy. Shows degeneration including in the eyes. |
| · Dmel\Glut1Scer\UAS.cBa * DmGluT1 |
DmGluT1
Glut1Scer\UAS.cBa |
FBal0256734 | Defects for locomotor behavior, climbing ability, and reduced lifespan. |
| · Dmel\BmcpScer\UAS.cBa * DmUCP5 |
DmUCP5
BmcpScer\UAS.cBa |
FBal0256733 | Defects for locomotor behavior, bang sensitive. Shows glial pathology, neuronal defects. Reduction in life expectancy. |
| For detailed information of drivers: http://flybase.org/search/disease/#/page/1 | |||