FlyBase Allele Report: Dmel\TER94[GD9777]

Expression of TER94^GD9777 under the control of Scer\GAL4^Hand.PU results in drastically shortened adult lifespan and severe morphological defects in the adult heart (the highly ordered packing of myofilaments in the heart is completely disrupted). Expression under the combined control of Scer\GAL4^tin.cBa and Scer\GAL4^Scer\UAS.cHa has no significant effect on either lifespan or cardiac performance of the adult flies.

Expressing TER94^GD9777 RNAi under the control of Scer\GAL4^{Hand.Switch.PU} and using the RU486 food supplementation to activate the RNAi only after eclosion also leads to reduced lifespan and although at 1 week of RNAi no heart morphological defects are observed, at 3 weeks the hearts show extensive disorganization of myofibrils or complete loss of sarcomeric material and this is accompanied by decreased cardiac performance compared to age-matched controls (reduced fractional shortening due to increased systolic diameter, shorter heart period).

(Viswanathan et al., 2016)

Expression of TER94^GD9777 under the control of Scer\GAL4^Mef2.PR results in mitochondrial morphology defects (round and swollen mitochondria) in larval muscles, deficit in larval locomotion (reduced crawling speed) and lethality as no viable adults eclose.

(Wang et al., 2016)

Expression of TER94^GD9777 RNAi under the control of Scer\GAL4^C57 disrupts lysosome tubule lattice and the fusion of autophagosome with the lysosome (judged from the failure of molecular markers to co-localize) in the sarcoplasm of third instar larval muscles. TER94^GD9777 expression leads to muscle wasting and severely impairs the ability of the larvae to move (not due to nervous system defects as synaptic transmission at neuromuscular junctions remains intact).

TER94^GD9777 RNAi driven by Scer\GAL4^C57 results in a dramatic accumulation of poly-ubiquitin aggregates in the cytoplasm of third instar larval muscle cells while the poly-ubiquitin conjugates normally observed around the cell nucleus are strongly depleted, suggesting a failed delivery of poly-ubiquitinated proteins to the proteasome. It also causes mitochondrial defects (with the mitochondria appearing swollen and dispersed rather than packed tubular structures) and the accumulation of lipofuscin granules that are not normally observed in wild-type.

(Johnson et al., 2015)

Scer\GAL4^hs.PU-mediated expression of TER94^GD9777 significantly attenuates SINV infection.

(Panda et al., 2013)

Expression of TER94^GD9777 in class IV neurons (ddaC) under the control of Scer\GAL4^ppk.PG causes a reduction in dendrite arborization, while major branches stay intact. These defects in class IV neurons mostly affect higher-order branches containing filamentous actin, but not primary dendrite branches rich in microtubules.

Expression of TER94^GD9777 in class III neurons (ddaA and ddaF) under the control of Scer\GAL4^19-12 affects the length of class III dendrites, although spike appearance is normal. Expression in a TER94^7-12 heterozygous background leads to a drastic reduction of the dendritic field and also induces lethality, as neurons are sometimes missing or display blebbing and fragmenting dendrites (drastic dendrite reduction or cell death occurs in approximately 37% of all neurons).

A high proportion of class IV neurons (ddaC) expressing TER94^GD9777 under the control of Scer\GAL4^ppk.PG retain long, attached dendrites (with 54% not severed).

Class III neurons overexpressing TER94^GD9777 under the control of Scer\GAL4^19-12 do not undergo apoptosis and are still present by 18 hours after puparium formation. In these flies, the ddaF neuron is more prone to survive than ddaA.

(Rumpf et al., 2011)

Adults expressing TER94^GD9777 under the control of the cardioblast-specific Scer\GAL4^tin.CΔ4 driver show significantly reduced survival on day 6 after a shift to 29[o]C compared to control flies.

(Neely et al., 2010)

Adults expressing TER94^GD9777 under the control of Scer\GAL4^elav.PLu (in the presence of Dcr-2^Scer\UAS.cDa to increase the efficiency of RNAi) do not show a significant defect in avoidance of noxious temperature (46[o]C) compared to control flies.

(Neely et al., 2010)

Depending on the insertion line used, expression under the control of Scer\GAL4^Mef2.PR can result in early pupal lethality or undefined lethality.

(Schnorrer et al., 2010)

Expression of TER94^GD9777 under the control of Scer\GAL4^Or22a.8197 results in a small but significant reduction in the number of olfactory receptor neuron axons in uninjured animals.

(Avery et al., 2009)

Expression under the control of Scer\GAL4^pnr-MD237 results in lethality before the pupal stage.

(Mummery-Widmer et al., 2009)

External Data

Linkouts

Bristle Screen Database (Knoblich Lab) - A database for RNAi phenotypes in bristle and notum development

9777

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

Scer\GAL4^bam.PU, TER94^GD9777 has abnormal size | male | adult stage phenotype, suppressible | partially by Sce^HMS05745, Scer\GAL4^bam.PU

(Butsch et al., 2023)

NOT suppressed by

Statement

Reference

Scer\GAL4^Mef2.PR, TER94^GD9777 has lethal - all die before end of P-stage phenotype, non-suppressible by clu^UAS.Tag:MYC/Scer\GAL4^Mef2.PR

(Wang et al., 2016)

Scer\GAL4^Mef2.PR, TER94^GD9777 has abnormal locomotor behavior | third instar larval stage phenotype, non-suppressible by clu^UAS.Tag:MYC/Scer\GAL4^Mef2.PR

(Wang et al., 2016)

Enhancer of

Statement

Reference

TER94^GD9777, Scer\GAL4^GMR.PU is an enhancer of visible | adult stage | progressive phenotype of Chchd2^S81L.UAS, Scer\GAL4^GMR.PU

(Baek et al., 2021)

Suppressor of

Statement

Reference

TER94^GD9777, Scer\GAL4^Or22a.8197 is a suppressor of abnormal neuroanatomy | conditional phenotype of Mmus\Wld^S.UAS, Scer\GAL4^Or22a.8197

(Avery et al., 2009)

NOT Suppressor of

Statement

Reference

sordd1^UAS.cXa, TER94^GD9777, Scer\GAL4^GMR.PU is a non-suppressor of visible | adult stage phenotype of Scer\GAL4^GMR.PU, ninaE^G69D.UAS.cXa

(Xu et al., 2020)

Phenotype Manifest In

NOT Enhanced by

Statement

Reference

Scer\GAL4^bam.PU, TER94^GD9777 has spermatozoon | absent phenotype, non-enhanceable by Sce^HMS05745, Scer\GAL4^bam.PU

(Butsch et al., 2023)

Scer\GAL4^bam.PU, TER94^GD9777 has male germ cell nucleus phenotype, non-enhanceable by Sce^HMS05745, Scer\GAL4^bam.PU

(Butsch et al., 2023)

Suppressed by

Statement

Reference

Scer\GAL4^bam.PU, TER94^GD9777 has testis phenotype, suppressible | partially by Sce^HMS05745, Scer\GAL4^bam.PU

(Butsch et al., 2023)

Scer\GAL4^bam.PU, TER94^GD9777 has spermatocyte cyst phenotype, suppressible by Sce^HMS05745, Scer\GAL4^bam.PU

(Butsch et al., 2023)

Scer\GAL4^bam.PU, TER94^GD9777 has spermatid phenotype, suppressible by Sce^HMS05745, Scer\GAL4^bam.PU

(Butsch et al., 2023)

Scer\GAL4^vas.PU, TER94^GD9777 has spermatid | germline clone | absent phenotype, suppressible | partially by Sce^KO

(Butsch et al., 2023)

Scer\GAL4^C57, TER94^GD9777 has lysosome | third instar larval stage phenotype, suppressible by Hsap\VCP^UAS.cCa, Scer\GAL4^C57

(Johnson et al., 2015)

Scer\GAL4^C57, TER94^GD9777 has embryonic/larval somatic muscle cell | third instar larval stage phenotype, suppressible by Hsap\VCP^UAS.cCa, Scer\GAL4^C57

(Johnson et al., 2015)

NOT suppressed by

Statement

Reference

Scer\GAL4^bam.PU, TER94^GD9777 has spermatozoon | absent phenotype, non-suppressible by Sce^HMS05745, Scer\GAL4^bam.PU

(Butsch et al., 2023)

Scer\GAL4^bam.PU, TER94^GD9777 has male germ cell nucleus phenotype, non-suppressible by Sce^HMS05745, Scer\GAL4^bam.PU

(Butsch et al., 2023)

Scer\GAL4^Mef2.PR, TER94^GD9777 has mitochondrion | third instar larval stage phenotype, non-suppressible by clu^UAS.Tag:MYC/Scer\GAL4^Mef2.PR

(Wang et al., 2016)

Enhancer of

Statement

Reference

TER94^GD9777, Scer\GAL4^GMR.PU is an enhancer of eye phenotype of Chchd2^S81L.UAS, Scer\GAL4^GMR.PU

(Baek et al., 2021)

Suppressor of

Statement

Reference

TER94^GD9777, Scer\GAL4^Or22a.8197 is a suppressor of olfactory receptor neuron | conditional phenotype of Mmus\Wld^S.UAS, Scer\GAL4^Or22a.8197

(Avery et al., 2009)

NOT Suppressor of

Statement

Reference

sordd1^UAS.cXa, TER94^GD9777, Scer\GAL4^GMR.PU is a non-suppressor of eye phenotype of Scer\GAL4^GMR.PU, ninaE^G69D.UAS.cXa

(Xu et al., 2020)

Other

Statement

Reference

Sce^HMS05745, Scer\GAL4^bam.PU, TER94^GD9777 has Nebenkern | absent phenotype

(Butsch et al., 2023)

Additional Comments

Genetic Interactions

Statement

Reference

The mitochondrial morphology defects in larval muscles, larval locomotion deficit and failure to produce viable adults observed upon Scer\GAL4^Mef2.PR-driven expression of TER94^GD9777 cannot be significantly rescued by co-expression of clu^UAS.Tag:MYC.

(Wang et al., 2016)

Xenogenetic Interactions

Statement

Reference

The disruption of sarcoplasmic lysosomal tubular network observed in muscles of third instar larvae expressing TER94^GD9777 RNAi under the control of Scer\GAL4^C57 is rescued by co-expression of Hsap\VCP^Scer\UAS.cCa.

(Johnson et al., 2015)

Co-expression of TER94^GD9777 suppresses the protective effect on axotomised olfactory receptor neurons in flies expressing Mmus\wld^S.Scer\UAS under the control of Scer\GAL4^Or22a.8197. An increased amount of Wallerian degeneration is seen 15 days after injury. No effect is seen in uninjured age-matched controls.

(Avery et al., 2009)

Complementation and Rescue Data

Comments

Images (0)

Mutant

Wild-type

Stocks (1)

VDRC

v24354

w¹¹¹⁸; P{GD9777}v24354

Notes on Origin

Discoverer