FlyBase Allele Report: Dmel\gl[60j]

gl^60j homozygous adults previously trained under 12h:12h light:dark cycles still maintain a rhythmic behavior under constant darkness conditions, but present a severe decrease in circadian phase shifting in response to light pulses during the late night period, as compared to controls.

(Ni et al., 2017)

Third instar eye discs in gl^60j mutants display reduced numbers of photoreceptor neuron precursors and disorganized cellular arrangement, compared with controls. gl^60j mutant photoreceptor precursors are not correctly recruited into the developing ommatidia in the third instar eye disc. Cellular organization of the retina in gl^60j mutants remains severely compromised through metamorphosis to adulthood, although photoreceptor neurons remain present, in contrast to previous reports.

The cell bodies of photoreceptor neurons in gl^60j mutants fail to elongate during metamorphosis.

The axonal projections of photoreceptor neurons in gl^60j mutants are highly disorganized, branch profusely, and innervate primarily the medulla of the optic lobe. Histaminergic projections are still present but are disorganized as compared to wild-type. gl^60j mutant photoreceptor neurons differentiate presynaptic specializations, but the synaptic vesicles are spread along the length of the axons, while in controls they accumulate at the distal tips of the axons. The lamina of the optic lobe is reduced in size in gl^60j mutants, as compared to controls.

Large gl^60j mutant clones in the developing eye do not acquire normal organization, fail to incorporate into the ommatidia, and re-localize to the basal side of the retina. This phenotype is not observed in small gl^60j clones.

(Bernardo-Garcia et al., 2016)

gl^60j mutants, like wild type flies, show arrhythmic behavior in constant dim white light conditions.

(Buhl et al., 2016)

gl^60j/gl^60j and gl³/gl^60j mutants possess fewer and fused ommatidia, with no presence of differentiated rhabdomeres, and boundaries between ommatidia are difficult to distinguish, as compared to wild type.

Both gl^60j/gl^60j mutant larvae and gl^60j/gl^60j clones in the third instar eye imaginal disc display disrupted photoreceptor cluster patterning, but no aberrant or excessive cell death in the retina field, as compared to wild type. At 48 h APF, gl^60j/gl^60j mutants possess all expected cell types, photoreceptors, cone and pigment cells, as compared to wild type, however no ommatidia contains the correct number of each retinal cell type, there is complete disruption of organization of retinal cells into distinct identifiable ommatidia, and cone and primary pigment cells are either too few or too many in number, and there is some evidence of cell death in photoreceptor cells. At 72 h APF, there is extensive cell death in the retinal field and in photoreceptor cells.

At 96 h APF, gl³/gl^60j mutants display increased cell death of photoreceptors in the retina.

(Liang et al., 2016)

gl^60j mutants exhibit abnormal light-dependent temperature preference. In contrast to wild-type, they prefer higher temperature in the dark than in the light.

gl^60j mutants not only have abnormal eye components, but also lack a subset of circadian clock cells, the posterior dorsal neurons (DN1[[p]]s).

(Head et al., 2015)

gl^60j mutants lack the majority of DN1 neurons except the two DN[1a]. The dorsal fusion commissure is thinner than in wild-type, probably as a result of loss of DNa projections.

(Helfrich-Forster et al., 2007)

When the locomotor activity of wild-type flies are monitored at 18 and 29^oC, an earlier evening peak is seen at 18^oC. This is not seen in mutants.

(Collins et al., 2004)

At high-light intensity, gl^60j flies are able to resynchronize to a shift in the light-dark schedule of 8 hours. However, at 1000-fold lower light intensity, gl^60j mutants take longer to synchronize to new schedules than wild-type flies. Entrained gl^60j flies significantly anticipate the light-ON transient, while wild-type flies do not.

Unlike wild-type flies, gl^60j flies do not show arrhythmia in response to constant light. These mutants are unable to entrain to red light-dark schedules, to which wild-type flies can entrain.

(Klarsfeld et al., 2004)

gl^60j mutants lack the ocelli, the ommatidial photoreceptors, the primary and secondary pigments of the eye, Bolwigs organ and the eyelet.

(Helfrich-Forster et al., 2002)

Third instar larvae have detectable dendritic arborisation of the lateral neurons in only 18% of cases and the average area of the arborisation is reduced compared to controls.

(Malpel et al., 2002)

Homozygous flies lack the Hofbauer-Buchner (H-B) eyelet cells. The morphology of the optic lobes is altered. There is a reduction in the Pdf-positive arborisations in the accessory medulla and the medulla. Mutant flies can entrain and reentrain to 12 hour light-12 hour dark (LD) cycles. The morning peak is less compact than in wild-type flies, is not as well entrained to the LD cycles and takes an average of 6 days to adapt to the new phase, whereas the evening peak adapts quickly. Flies show 100% rhythmicity under LD conditions. Most flies become arrhythmic under constant light conditions.

(Helfrich-Forster et al., 2001)

Wild-type larvae reduce their path lengths when exposed to light. This response is severely reduced in gl^60j larvae. Wild-type larvae show increased head swinging when exposed to light. This response is abolished in gl^60j larvae. Wild-type larvae show a greater change in direction when lights are turned on or off (light (L) to dark (D), or D to L transition) than in the absence of a light transition (D to D). The amplitude of change of direction is greater for the D to L than for the L to D transition. This difference in the amplitude of change of direction between the D to L and L to D transitions is abolished in gl^60j larvae, although change of direction in the absence of a light transition (D to D) is still significantly lower than for either the D to L and L to D transition.

(Busto et al., 1999)

Only a few loosely clustered photoreceptors can be seen without formation of a larval optic nerve. LP1 cells show abnormal neuronal processes but no clear Ddc arborisation can be detected.

(Mukhopadhyay and Campos, 1995)

Eye phenotype.

(O'Neill et al., 1995)

Third instar foraging and wandering stage larvae fail to respond to light.

(Sawin-McCormack et al., 1995)

Displays locomotor activity rhythm with an approximately 24h period.

(Vosshall and Young, 1995)

gl^60j males that are also mutant for mle⁴ show darker eye pigmentation than their mle⁴/+ sibs.

(Hiebert and Birchler, 1994)

Pattern of retinal axon projections in the larval brain is completely disorganised. Axon fascicles take aberrant trajectories after they exit the optic stalk and terminate in ectopic locations often outside the lamina target area.

(Kunes et al., 1993)

Photoreceptor axons project to the brain aberrantly in late third instar larvae. This phenotype is variable. There is a variable pattern of S phase cells located between the outer proliferative centre and inner proliferative centre, in the region where the lamina precursor cells normally reside.

(Selleck and Steller, 1991)

Strong allele. The eye is disorganised. Corneal hairs and red pigment granules are only present in the centre of the eye. The ocellar lenses are normal in size, but lack the bulge of the wild-type, and have small protuberances. The lenses of the compound eye and ocelli are roughened with "corneal nipples".

(Stark and Carlson, 1991)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

gl^60j has photoperiod response variant | adult stage phenotype, enhanceable by Rh7¹/Rh7¹

(Ni et al., 2017)

gl^60j has abnormal locomotor rhythm phenotype, enhanceable by cry^b

(Klarsfeld et al., 2004)

Suppressed by

Statement

Reference

gl^60j has increased cell death | P-stage phenotype, suppressible by BacA\p35^UAS.cUa/Scer\GAL4^so.PU

(Liang et al., 2016)

gl^60j has increased cell death | P-stage phenotype, suppressible by BacA\p35^UAS.cUa/Scer\GAL4^hs.PU

(Liang et al., 2016)

NOT suppressed by

Statement

Reference

gl^60j has visible | adult stage phenotype, non-suppressible by Pph13^hs.PL

(Liang et al., 2016)

gl^60j has visible | adult stage phenotype, non-suppressible by BacA\p35^UAS.cUa/Scer\GAL4^so.PU

(Liang et al., 2016)

gl^60j has visible | adult stage phenotype, non-suppressible by BacA\p35^UAS.cUa/Scer\GAL4^hs.PU

(Liang et al., 2016)

Enhancer of

Statement

Reference

gl^60j/gl^60j is an enhancer of photoperiod response variant | adult stage phenotype of Rh7¹

(Ni et al., 2017)

gl^60j is an enhancer of abnormal circadian rhythm phenotype of so¹

(Helfrich-Forster et al., 2002)

Suppressor of

Statement

Reference

gl^60j is a suppressor of photoperiod response variant phenotype of cry^b

(Klarsfeld et al., 2004)

gl^60j/gl[+] is a suppressor of visible phenotype of Pp2B-14D^act.GMR

(Sullivan and Rubin, 2002)

NOT Suppressor of

Statement

Reference

gl^60j is a non-suppressor of photoperiod response variant phenotype of Pdf⁰¹

(Klarsfeld et al., 2004)

gl^60j is a non-suppressor of abnormal locomotor rhythm phenotype of Pdf⁰¹

(Klarsfeld et al., 2004)

Other

Statement

Reference

Rh7¹, gl^60j has abnormal circadian rhythm | adult stage phenotype

(Ni et al., 2017)

cry^b, gl^60j has abnormal locomotor rhythm phenotype

(Helfrich-Forster et al., 2001)

Phenotype Manifest In

NOT Enhanced by

Statement

Reference

gl^60j has retina | P-stage | somatic clone phenotype, non-enhanceable by Blimp-1¹⁷/Blimp-1¹⁷

(Wang et al., 2022)

Suppressed by

Statement

Reference

gl^60j has eye photoreceptor cell | P-stage phenotype, suppressible by gl^hs.PL/Pph13^hs.PL

(Liang et al., 2016)

gl^60j has rhabdomere phenotype, suppressible by gl^hs.PL/Pph13^hs.PL

(Liang et al., 2016)

NOT suppressed by

Statement

Reference

gl^60j has retina | somatic clone | P-stage phenotype, non-suppressible by Blimp-1¹⁷/Blimp-1¹⁷

(Wang et al., 2022)

gl^60j has ommatidium | adult stage phenotype, non-suppressible by BacA\p35^UAS.cUa/Scer\GAL4^hs.PU

(Liang et al., 2016)

gl^60j has eye photoreceptor cell | adult stage phenotype, non-suppressible by BacA\p35^UAS.cUa/Scer\GAL4^so.PU

(Liang et al., 2016)

gl^60j has eye photoreceptor cell | adult stage phenotype, non-suppressible by BacA\p35^UAS.cUa/Scer\GAL4^hs.PU

(Liang et al., 2016)

gl^60j has eye photoreceptor cell | P-stage phenotype, non-suppressible by Pph13^hs.PL

(Liang et al., 2016)

gl^60j has eye phenotype, non-suppressible by Pph13^hs.PL

(Liang et al., 2016)

gl^60j has eye phenotype, non-suppressible by BacA\p35^UAS.cUa/Scer\GAL4^so.PU

(Liang et al., 2016)

gl^60j has eye phenotype, non-suppressible by BacA\p35^UAS.cUa/Scer\GAL4^hs.PU

(Liang et al., 2016)

gl^60j has ommatidium | adult stage phenotype, non-suppressible by BacA\p35^UAS.cUa/Scer\GAL4^so.PU

(Liang et al., 2016)

Enhancer of

Statement

Reference

gl^60j is an enhancer of eye phenotype of so¹

(Helfrich-Forster et al., 2002)

NOT Enhancer of

Statement

Reference

gl^60j is a non-enhancer of phenotype of Doa⁷/Doa^HD

(Yun et al., 2000)

gl^60j is a non-enhancer of phenotype of Doa^HD/Doa^Dem

(Yun et al., 2000)

Suppressor of

Statement

Reference

gl^60j/gl[+] is a suppressor of eye phenotype of Pp2B-14D^act.GMR

(Sullivan and Rubin, 2002)

NOT Suppressor of

Statement

Reference

gl^60j is a non-suppressor of phenotype of Doa⁷/Doa^HD

(Yun et al., 2000)

gl^60j is a non-suppressor of phenotype of Doa^HD/Doa^Dem

(Yun et al., 2000)

Additional Comments

Genetic Interactions

Statement

Reference

Rh7¹, gl^60j double homozygous adults previously trained under 12h:12h light:dark cycles display both an increased proportion of arrhythmic individuals under constant darkness conditions and increased delay in circadian phase shifting to a 8h delay in the light:dark transition, as compared to either single homozygote.

(Ni et al., 2017)

Pulsing Pph13^hs.PL expression using heat shocks does not rescue photoreceptor differentiation in gl^60j/gl^60j mutant retinas at 96 h APF, and does not further disrupt or rescue overall eye morphology of gl^60j/gl^60j mutants.

Pulsing expression of both Pph13^hs.PL and gl^hs.PL using heat shocks restores photoreceptor differentiation in gl^60j/gl^60j mutant) retinas, as indicated by the presence of definable rhabdomeres at 96 h APF.

(Liang et al., 2016)

gl^60j, cry^b flies fail to entrain to light-dark cycles of even the highest amplitude.

gl^60j, Pdf⁰¹ flies show similar weak short-period rhythmicity phenotypes when kept in constant darkness to Pdf⁰¹ single mutant flies.

(Klarsfeld et al., 2004)

gl^60j; so¹ double mutants are completely eyeless and the eyelet is absent. These double mutants can only re-entrain to wavelengths shorter than 450nm, while so¹ single mutants can entrain to wavelengths up to 550nm. Unlike so¹ single mutants, phase relationship the evening peak activity of gl^60j; so¹ double mutants is not dependent on wavelength and these flies rarely show antidromic phase shifting.

(Helfrich-Forster et al., 2002)

The rough eye phenotype of Pp2B-14D^act.GMR flies is strongly suppressed by one copy of gl^60j.

(Sullivan and Rubin, 2002)

gl^60j cry^b double mutant flies do not entrain at all to 12 hour light-12 hour dark (LD) cycles. At 100 lux, approximately 70% of the flies show free-running behaviour. The average activity shows a small peak after lights off at 100 lux and at 1000 lux virtually all flies react to lights off with a pronounced activity peak. At 1000 lux, the activity level is generally lower during the light phase than during the dark phase. A free-running circadian activity component is present in 81% of the activity records, and after transfer into constant darkness conditions rhythmic locomotor behaviour usually continues from this free-running component and not from the lights-off peak. Approximately 30% of gl^60j cry^b double mutant flies show poor rhythmicity, even under LD conditions. At 100 lux, about 20% of the flies are arrhythmic, and about 10% show a complex rhythmicity characterised by several small but significant peaks in the periodograms. gl^60j cry^b double mutants show neither period changes nor any increase in activity level or intervals between morning and evening locomotor activity peaks after transfer from constant darkness to constant light conditions.

(Helfrich-Forster et al., 2001)

Weak suppressor of the rough eye phenotype caused by two insertions of P{GMR-Rho1}.

(Hariharan et al., 1995)

Xenogenetic Interactions

Statement

Reference

Expression of BacA\p35^Scer\UAS.cUa under the control of Scer\GAL4^so.PU or Scer\GAL4^hs.PU results in a decrease in cell death at 48 h APF, but did not rescue the eye morphology, retina structure, or photoreceptor differentiation defects of gl^60j/gl^60j mutants.

(Liang et al., 2016)

Complementation and Rescue Data

Rescued by

gl^60j is rescued by gl^+t9954

(Head et al., 2015)

gl^60j is rescued by gl^+t9954

(Busto et al., 1999)

gl^60j is rescued by gl^N432

(O'Neill et al., 1995)

gl^60j is rescued by gl^+t9954

(Sawin-McCormack et al., 1995)

Partially rescued by

gl³/gl^60j is partially rescued by gl^GFP.FPTB

(Liang et al., 2016)

gl^60j is partially rescued by gl^GFP.FPTB

(Liang et al., 2016)

gl^60j is partially rescued by gl^hs.PL

(Liang et al., 2016)

Comments

Periodic pulses after 24 h APF of gl^hs.PL using heat shocks neither rescues or induces additional defects with respect to eye morphology, but restores photoreceptor differentiation in gl^60j/gl^60j mutant retinas, as indicated by the presence of rhabdomeres separated by a distinct inter-rhabdomeral space, although many of these ommatidia still do not contain the full complement of eight photoreceptors.

Expression of a single copy of gl^{T:Avic\GFP-SF,T:Zzzz\FLAG,T:Zzzz\PSP.CS,T:Zzzz\TEV.CS,T:Zzzz\BLRP} rescues the overall external morphology of the eye, but not the photoreceptor differentiation defects of adult gl³/gl^60j and gl^60j/gl^60j mutants. In gl^60j/gl^60j mutants at 48 h APF, expression of a single copy of gl^{T:Avic\GFP-SF,T:Zzzz\FLAG,T:Zzzz\PSP.CS,T:Zzzz\TEV.CS,T:Zzzz\BLRP} significantly increases the number of ommatidia with the correct numbers of photoreceptor and cone cells.

Expression of two copies of gl^{T:Avic\GFP-SF,T:Zzzz\FLAG,T:Zzzz\PSP.CS,T:Zzzz\TEV.CS,T:Zzzz\BLRP} rescues the external morphology of the eye and photoreceptor differentiation defects of gl^60j/gl^60j mutants.

(Liang et al., 2016)

Normal light-dependent temperature preference and DN1p neurons are restored in gl^60j mutants by gl^+t9954.

(Head et al., 2015)

Images (0)

Mutant

Wild-type

Stocks (3)

Bloomington

509

gl^60j

6333

w^*; P{neoFRT}82B gl^60j

Kyoto

105949

gl^60j

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (7)

Reported As

Symbol Synonym

gl60j

(Fogle et al., 2015)

gl^60J

(Rosenzweig et al., 2008, Klarsfeld et al., 2004, Sullivan and Rubin, 2002, Foster and Helfrich-Förster, 2001, Campos et al., 1995, Sawin-McCormack et al., 1995)

gl^60j9

(Hiebert and Birchler, 1994)

gl^60j

(Wang et al., 2022, Zelhof et al., 2020, Morrison et al., 2018, Bernardo-Garcia et al., 2017, Lamaze et al., 2017, Ni et al., 2017, Bernardo-Garcia et al., 2016, Buhl et al., 2016, Liang et al., 2016, Head et al., 2015, Dolezelova et al., 2007)

gl^J60

(Sullivan and Rubin, 2002)

glass^60J

(Nandakumar et al., 2020)

glass^60j

(Yadlapalli et al., 2018, Helfrich-Forster et al., 2007, Shafer et al., 2006)

Name Synonyms

Secondary FlyBase IDs

References (50)

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