FlyBase Allele Report: Dmel\gbb[1]

Mutants show loss of expression of P{FMRFa-EGFP.Tv}, a marker for the six Ap4 neurons in the developing ventral nerve cord, and loss of expression of eya, which identifies the four Ap cluster neurons.

(Bivik et al., 2015)

The amplitude of spontaneous miniature excitatory junction potentials (mEJPs) at the neuromuscular junction is not significantly different from controls in gbb¹/gbb² larvae, while the mEJP frequency is significantly decreased. There is a significant decrease in evoked EJP amplitude and in quantal content in the mutant larvae.

gbb¹/gbb² larvae show a decrease in the number of boutons per neuromuscular junction compared to controls.

gbb¹/gbb² larvae show defects in synaptic vesicle cycling (as assayed using uptake and unloading of the dye FM1-43), showing modest defects in endocytosis and more marked defects in exocytosis.

(James et al., 2014)

gbb¹/gbb² mutant larvae have a reduced number of NMJ boutons compared to controls.

(Sulkowski et al., 2014)

Heterozygotes do not display defects in neuromuscular junction expansion.

(James and Broihier, 2011)

Homozygous gbb¹ mutant larvae are transparent and slightly smaller compared to wild-type larvae of the same developmental stage. This transparency is primarily due to a change in opacity of the fat body. All regions of the fat body are present in gbb¹ mutant larvae, however, the size of individual cells is reduced such that the entire organ is somewhat smaller in overall size.

Late third instar gbb¹/gbb³ mutant wing imaginal discs are 50% smaller in overall area compared to the area of wild-type wing discs of the same developmental stage.

gbb¹/gbb³ mutant larvae do not show a significant difference in overall protein levels compared to wild-type third instar larvae when normalised for body mass.

Homozygous gbb¹ third instar larvae have lower levels of lipids, triacylglycerides and short-chain fatty acids compared to wild-type larvae.

gbb¹/gbb³ mutant third instar larvae have lower levels of glucose and trehalose levels than wild-type controls.

gbb¹/gbb³ mutant third instar larvae show increased uptake and transport of ingested fluorescently labeled fatty acids from the midgut lumen to the fat body compared to wild-type controls.

(Ballard et al., 2010)

gbb¹ homozygous mutants exhibit significantly reduced synaptic currents in aCC/RP2 compared with heterozygous controls.

(Fradkin et al., 2008)

Large double-sided gbb¹ clones in the anterior compartment of the wing lead to non-autonomous defects in the posterior compartment. These clones show a narrowing of the L4-L5 intervein and a truncation of wing vein L5. Wings containing both large anterior and posterior gbb¹ clones exhibit a more severe patterning defect than a clone in either compartment alone, including a complete loss of L5 and defects in L4 specification.

The wings of gbb¹/gbb⁴ flies show a loss of the L4-L5 intervein and a truncation of wing vein L5.

gbb¹ clones induced in the anterior of the wing produces defects in the specification of the L4-L5 intervein and the L5 vein.

(Bangi and Wharton, 2006)

The evoked synaptic current amplitude recorded in aCC/RP2 neurons is significantly smaller in gbb¹ homozygotes compared with heterozygous controls.

(Baines, 2004)

gbb¹/gbb⁴ mutants exhibit a slight but consistent reduction in neurotransmitter release (measured by intracellular recordings from muscle 6 of segment A3). These mutants also show a small reduction in synaptic bouton number. Gross synaptic ultrastructure (examined in 3rd instar larval muscles 6 & 7) appears normal apart from a small population of large vesicles distinct from and unlike synaptic vesicles, and occasional aberrant cytoplasmic electron-dense structures ('T-bodies') that can cluster synaptic vesicles. In the active zones of gbb¹/gbb⁴ mutants there are intermittent detachments between pre- and postsynaptic membranes. Mutant boutons are approximately the same size as wild-type boutons but the bouton surface area per active zone is increased. However, the bouton surface area per T bar is decreased compared to wild-type. The wings of gbb¹/gbb⁴ adults lack a posterior crossvein, and have a truncated L5 vein. Very few gbb¹/gbb² animals survive to the 3rd instar larval stage. Synapse size and bouton density are greatly reduced at neuromuscular junctions in gbb¹/gbb²; P{UAS-gbb.K}9.9 larvae compared to wild-type. There is a severe decrease in the amplitude of evoked excitatory junctional potentials (EJP) in this mutant combination when compared to wild-type. The mutants also show a small increase in mini-EJP amplitude and a reduction in the frequency of spontaneous release when compared to wild-type. Measurements of quantal content of these mutant synapses shows that they release 4-fold less neurotransmitter than wild-type synapses.

(McCabe et al., 2003)

gbb¹/gbb⁴ males raised at 18^oC have significantly smaller testes than normal, with a dramatic reduction in the number of germ cells of all stages, particularly germ line stem cells, spermatogonia and spermatocytes. In the most extreme cases, germ line stem cells, spermatogonia and spermatocytes are completely missing.

(Shivdasani and Ingham, 2003)

gbb¹/gbb⁴ adults lack the posterior crossvein (PCV) and the distal tips of veins L4 and L5. The overall size of the wing is reduced compared to wild type. Homozygous clones in the wing disc show the same size, distribution and frequency as control wild-type clones. Mutant phenotypes are only observed in clones or regions of clones where both the dorsal and ventral surfaces of the wing are mutant (referred to as "double-sided" clones). Double-sided clones that occupy the entire posterior compartment of the wing show loss of the PCV and loss of the distal quarter of vein L5. Smaller clones covering either just the PCV or distal tip of L5 also show loss of the corresponding vein structures. In double-sided clones that cover only the anterior or posterior half of the PCV, the vein is absent in the mutant cells and stops either precisely at the boundary of the dorsoventral overlap or within 2 to 3 cells of it. The PCV can stop on either the wild-type or the mutant side of the clone boundary. This partial loss of the PCV is only seen if the double-sided clone includes at least one of the two junctions of the PCV with the longitudinal veins. Double-sided clones that fall within the distal quarter of L5 show loss of the vein only within mutant tissue, with the vein stopping within 2 to 3 cells of the dorsoventral overlap of the clone. The distal tip of L5 can also be missing in cases where clones cover the proximal part of L5, even if the distal quarter of L5 is wild-type (on either ventral, dorsal or both surfaces). Double-sided clones that cover the entire posterior compartment of the wing have little or no effect on vein L4. Loss of L4 is seen when double-sided clones cover the region both anterior and posterior to the vein. Double-sided clones that cover the entire anterior compartment of the wing have no defects in the costal vein or veins L1, L2 or L3. These clones are associated with a reduction in overall size of the wing blade (both the anterior and posterior compartments show a reduction in size) and loss of all but the most proximal portion of vein L5. The truncation of L5 is somewhat variable and may or may not be accompanied by the loss of the PCV. Double-sided clones that cover the region between veins L1 and L3, or the region between L3 and L4 (but not including L3) are normal in size and patterning. Double-sided clones with an anterior border in the intervein region between L2 and L3 and a posterior border running the length of the A/P compartment boundary show the mutant phenotypes seen in clones occupying the whole anterior compartment.

(Ray and Wharton, 2001)

gbb¹/gbb⁴ flies show wing vein truncations.

(Yu et al., 2000)

Less than 10% of mutants dies as embryos. Females with homozygous gbb¹ germ line clones produce phenotypically wild type eggs that hatch and survive to adulthood. Mutant larvae are lethargic and flaccid. Imaginal discs are dramatically reduced. Fat body morphology is abnormal, giving rise to transparent phenotype. Cuticle exhibits defects in the telson region. In severe cases posterior spiracles do not protrude from the larval bosy and the stigmatophores are partially fused and more dorsally situated. In embryogenesis, formation of the anterior midgut constriction starts but fails to reach completion, giving rise to a bulbous anterior midgut. The position of the other constrictions is shifted. Mutants fail to extend the gastric caecae by stage 17. The eyes of gbb¹/gbb⁴ are reduced in size with 10-20% ommatidia fewer than wild type. Loss of ommatidia is restricted to the ventral portion of the eye. gbb¹/gbb⁴ show extra scutellar and dorsocentral bristles. Ectopic scutellars most often occur in close proximity to the endogenous bristle, but sometimes between the anterior and posterior scutellar bristles.

(Wharton et al., 1999)

Less than 5% of gbb¹/gbb⁴ flies survive to adulthood at 25^oC. Escapers show a reduction of wing veins L4 and L5 and lack the posterior crossvein.

(Haerry et al., 1998)

Homozygous embryos show defects in gut morphogenesis and die as early larvae. gbb¹/gbb⁴ animals generally die as larvae, with rare adult escapers (less than 1%). The larvae appear transparent, due to a defect both in the quantity and quality of the fat body, and a dramatic reduction in imaginal tissues. Areas of the brain are also reduced. The larvae develop more slowly than wild-type and never attain wild-type size. Adult escapers have small, misshapen wings, which lack the posterior crossvein, much of wing vein L5, distal portions of vein L4 and the posterior half of the anterior crossvein. There is a loss of intervein material, especially between veins L2 and L3, between L4 and L5 and posterior to L5, resulting in narrow, pointed wings. Thinning of vein L2 and some ectopic vein material in the intervein region flanking vein L2 is common. No abnormalities in position or type of wing bristles are seen along the wing margin, although ectopic margin bristles are often seen along a vein or in intervein tissue in distal regions of the wing. The eyes are smaller than normal and have supernumerary vibrissae, there is an increase in the number of thoracic bristles, and leg segments may be misshapen. Female sterility is also seen. Homozygous clones are not recovered in the wing if the clones are induced before 36 hours after egg laying. Clones in the wing are recovered if they are induced later. Clones located in both the anterior and posterior compartments, as well as clones limited to the posterior compartment, show defects in wing pattern elements, including loss of the posterior crossvein, loss of portions of veins L4 and L5, and loss of the distal part of vein L3 at the wing margin. 80% of these clones that show a mutant phenotype cover a portion of the wing where vein material is normally located. Clones strictly limited to the anterior compartment or along the anterior/posterior (A/P) boundary show no wing defects, with the exception of very small clones located near the anterior crossvein, which result in ectopic vein material anterior to vein L3. Wing vein loss is sometimes seen in wild-type tissue at a distance from the clone in wings containing multiple clones; one in the posterior compartment and another along the A/P boundary.

(Khalsa et al., 1998)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

NOT Enhanced by

Statement

Reference

gbb²/gbb¹ has abnormal neuroanatomy phenotype, non-enhanceable by Neto[+]/Neto³⁶

(Sulkowski et al., 2014)

gbb¹ has lethal | recessive phenotype, non-enhanceable by lilli^unspecified

(Su et al., 2001)

Suppressed by

Statement

Reference

gbb⁴/gbb¹ has visible phenotype, suppressible by Agam\gbb1^gbb.PF

(Fritsch et al., 2010)

gbb⁴/gbb¹ has visible phenotype, suppressible by Agam\gbb2^gbb.PF

(Fritsch et al., 2010)

gbb⁴/gbb¹ has visible phenotype, suppressible by sax¹/Agam\gbb1^gbb.PF/sax²

(Fritsch et al., 2010)

gbb⁴/gbb¹ has visible phenotype, suppressible by sax¹/Agam\gbb2^gbb.PF/sax²

(Fritsch et al., 2010)

gbb¹ has abnormal neurophysiology phenotype, suppressible by Dys^Dp186.166.3

(Fradkin et al., 2008)

gbb¹ has lethal | recessive phenotype, suppressible by Dp(2;2)B16

(Ray and Wharton, 2001)

gbb¹ has lethal | recessive phenotype, suppressible by Dp(2;2)B16/Dp(2;2)DTD48

(Ray and Wharton, 2001)

gbb¹ has lethal | recessive phenotype, suppressible by Dp(2;2)DTD48

(Ray and Wharton, 2001)

gbb⁴/gbb¹ has lethal phenotype, suppressible | partially by Dp(2;2)B16/Dp(2;2)DTD48

(Ray and Wharton, 2001)

gbb⁴/gbb¹ has lethal phenotype, suppressible | partially by Dp(2;2)DTD48

(Ray and Wharton, 2001)

gbb⁴/gbb¹ has lethal phenotype, suppressible | partially by Dp(2;2)B16

(Ray and Wharton, 2001)

NOT suppressed by

Statement

Reference

gbb⁴/gbb¹ has visible phenotype, non-suppressible by sax¹/scw^gbb.PF/sax²

(Fritsch et al., 2010)

gbb¹ has abnormal neurophysiology | recessive phenotype, non-suppressible by Scer\GAL4^eve.RN2/rut^UAS.cZa

(Baines, 2004)

Enhancer of

Statement

Reference

gbb¹ is an enhancer of partially lethal - majority die phenotype of Neto¹⁰⁹

(Sulkowski et al., 2014)

gbb¹/gbb[+] is an enhancer of visible phenotype of dpp^d5/dpp^hr56

(Bangi and Wharton, 2006)

gbb¹/gbb[+] is an enhancer of visible | dominant phenotype of sog^EP7

(Araujo et al., 2003)

gbb¹ is an enhancer of visible | recessive phenotype of tkv⁴²⁷

(Khalsa et al., 1998)

NOT Enhancer of

Statement

Reference

gbb¹/gbb[+] is a non-enhancer of abnormal neurophysiology phenotype of Dys^Dp186.166.3

(Fradkin et al., 2008)

gbb¹ is a non-enhancer of abnormal neurophysiology phenotype of Dys^Dp186.UAS, Scer\GAL4^eve.RN2

(Fradkin et al., 2008)

gbb¹/gbb[+] is a non-enhancer of visible | dominant phenotype of sog^EP11

(Araujo et al., 2003)

Suppressor of

Statement

Reference

gbb¹/gbb[+] is a suppressor of abnormal neuroanatomy | third instar larval stage phenotype of Scer\GAL4^Gli-rL82, mav^UAS.GFP

(Fuentes-Medel et al., 2012)

gbb⁴/gbb¹ is a suppressor of abnormal neuroanatomy phenotype of spict^mut

(Wang et al., 2007)

gbb¹/gbb[+] is a suppressor | partially of abnormal neuroanatomy phenotype of spict^mut

(Wang et al., 2007)

gbb¹ is a suppressor of abnormal neurophysiology phenotype of Scer\GAL4^eve.RN2, rut^UAS.cZa

(Baines, 2004)

NOT Suppressor of

Statement

Reference

gbb¹/gbb[+] is a non-suppressor of abnormal neurophysiology phenotype of Dys^Dp186.166.3

(Fradkin et al., 2008)

gbb¹ is a non-suppressor of abnormal neurophysiology phenotype of Dys^Dp186.UAS, Scer\GAL4^eve.RN2

(Fradkin et al., 2008)

Other

Statement

Reference

Neto³⁶, gbb¹/gbb[+] has abnormal neuroanatomy phenotype

(Sulkowski et al., 2014)

RhoGAP92B¹, gbb¹/gbb[+] has abnormal neuroanatomy | dominant | third instar larval stage phenotype

(Nahm et al., 2010)

gbb¹, gbb^UAS.cKa has abnormal neurophysiology | heat sensitive phenotype

(Baines, 2004)

gbb⁴/gbb¹, sax⁴ has partially lethal phenotype

(Khalsa et al., 1998)

gbb⁴/gbb¹, sax⁵ has partially lethal phenotype

(Khalsa et al., 1998)

dpp^s4/dpp^d6, gbb¹ has visible phenotype

(Khalsa et al., 1998)

dpp^s4/dpp^d6, gbb¹ has partially lethal phenotype

(Khalsa et al., 1998)

Phenotype Manifest In

Enhanced by

Statement

Reference

gbb¹ has crossvein | somatic clone phenotype, enhanceable by dpp^d12/dpp[+]

(Bangi and Wharton, 2006)

gbb¹ has wing vein L5 phenotype, enhanceable by dpp^d12

(Khalsa et al., 1998)

gbb¹ has wing cell phenotype, enhanceable by dpp^d12

(Khalsa et al., 1998)

gbb¹ has submarginal cell phenotype, enhanceable by dpp^d12

(Khalsa et al., 1998)

gbb¹ has 2nd posterior cell phenotype, enhanceable by dpp^d12

(Khalsa et al., 1998)

gbb¹ has discal cell phenotype, enhanceable by dpp^d12

(Khalsa et al., 1998)

gbb¹ has wing basal cell 2 phenotype, enhanceable by dpp^d12

(Khalsa et al., 1998)

gbb¹ has anterior crossvein phenotype, enhanceable by dpp^d12

(Khalsa et al., 1998)

gbb¹ has wing phenotype, enhanceable by Df(2L)tkv2

(Khalsa et al., 1998)

gbb¹ has wing vein L4 phenotype, enhanceable by dpp^d12

(Khalsa et al., 1998)

gbb¹ has wing vein L2 phenotype, enhanceable by dpp^d12

(Khalsa et al., 1998)

gbb¹ has wing vein L3 phenotype, enhanceable by dpp^d12

(Khalsa et al., 1998)

NOT Enhanced by

Statement

Reference

gbb²/gbb¹ has terminal bouton phenotype, non-enhanceable by Neto[+]/Neto³⁶

(Sulkowski et al., 2014)

gbb¹ has wing vein L5 | somatic clone phenotype, non-enhanceable by dpp^d12/dpp[+]

(Bangi and Wharton, 2006)

gbb¹ has crossvein | somatic clone phenotype, non-enhanceable by dpp^s4/dpp[+]

(Bangi and Wharton, 2006)

gbb¹ has wing vein L5 | somatic clone phenotype, non-enhanceable by dpp^s4/dpp[+]

(Bangi and Wharton, 2006)

Suppressed by

Statement

Reference

gbb⁴/gbb¹ has wing vein phenotype, suppressible by Agam\gbb1^gbb.PF

(Fritsch et al., 2010)

gbb⁴/gbb¹ has wing vein phenotype, suppressible by Agam\gbb2^gbb.PF

(Fritsch et al., 2010)

gbb⁴/gbb¹ has wing vein phenotype, suppressible by sax¹/Agam\gbb1^gbb.PF/sax²

(Fritsch et al., 2010)

gbb⁴/gbb¹ has wing vein phenotype, suppressible by sax¹/Agam\gbb2^gbb.PF/sax²

(Fritsch et al., 2010)

NOT suppressed by

Statement

Reference

gbb⁴/gbb¹ has wing vein phenotype, non-suppressible by sax¹/scw^gbb.PF/sax²

(Fritsch et al., 2010)

Enhancer of

Statement

Reference

gbb¹/gbb[+] is an enhancer of crossvein phenotype of dpp^d5/dpp^hr56

(Bangi and Wharton, 2006)

gbb¹/gbb[+] is an enhancer of wing vein L2 phenotype of dpp^d5/dpp^hr56

(Bangi and Wharton, 2006)

gbb¹/gbb[+] is an enhancer of wing vein L2 phenotype of dpp^d5/dpp^hr4

(Bangi and Wharton, 2006)

gbb¹/gbb[+] is an enhancer of wing vein phenotype of sog^EP7

(Araujo et al., 2003)

gbb¹ is an enhancer of wing vein phenotype of tkv⁴²⁷

(Khalsa et al., 1998)

NOT Enhancer of

Statement

Reference

gbb¹/gbb[+] is a non-enhancer of wing vein phenotype of sog^EP11

(Araujo et al., 2003)

Suppressor of

Statement

Reference

gbb¹/gbb[+] is a suppressor of bouton | third instar larval stage phenotype of Scer\GAL4^Gli-rL82, mav^UAS.GFP

(Fuentes-Medel et al., 2012)

gbb¹/gbb[+] is a suppressor of embryonic/larval neuromuscular junction | third instar larval stage phenotype of Scer\GAL4^Gli-rL82, mav^UAS.GFP

(Fuentes-Medel et al., 2012)

gbb¹/gbb[+] is a suppressor | partially of type I bouton | increased number | third instar larval stage phenotype of cmpy^Δ8

(James and Broihier, 2011)

gbb¹/gbb[+] is a suppressor of wing vein | ectopic phenotype of MAN1^ΔC

(Wagner et al., 2010)

gbb¹/gbb[+] is a suppressor of posterior crossvein phenotype of MAN1^ΔC

(Wagner et al., 2010)

gbb⁴/gbb¹ is a suppressor of embryonic/larval neuromuscular junction phenotype of spict^mut

(Wang et al., 2007)

gbb¹/gbb[+] is a suppressor | partially of embryonic/larval neuromuscular junction phenotype of spict^mut

(Wang et al., 2007)

gbb¹ is a suppressor of anterior crossvein phenotype of dpp^s4/dpp^d6

(Khalsa et al., 1998)

Other

Statement

Reference

Neto³⁶, gbb¹/gbb[+] has embryonic/larval neuromuscular junction phenotype

(Sulkowski et al., 2014)

Neto³⁶, gbb¹/gbb[+] has terminal bouton phenotype

(Sulkowski et al., 2014)

RhoGAP92B¹, gbb¹/gbb[+] has NMJ bouton | third instar larval stage phenotype

(Nahm et al., 2010)

dpp^d12, gbb⁴/gbb¹ has prothoracic tarsal segment | male phenotype

(Khalsa et al., 1998)

dpp^d12, gbb¹ has prothoracic tarsal segment | male phenotype

(Khalsa et al., 1998)

dpp^s4/dpp^d6, gbb¹ has wing phenotype

(Khalsa et al., 1998)

Additional Comments

Genetic Interactions

Statement

Reference

Syx4⁷³/+;gbb¹/+ double heterozygotic third instar larvae do not show significant differences in bouton number at the neuromuscular junction compared to wild type or single heterozygotes.

(Harris et al., 2016)

The ability of gbb^Scer\UAS.cKa expressed under the control of Scer\GAL4^Toll-6-D42 to rescue the electrophysiological defects seen at the neuromuscular junction in gbb¹/gbb² larvae is impaired but not completely abolished if the larvae are also homozygous for cmpy^Δ8.

(James et al., 2014)

One copy of Neto³⁶ does not enhance the reduction in NMJ bouton number seen in gbb¹/gbb² mutant larvae.

Larvae that are heterozygous for both Neto³⁶ and gbb¹ have smaller NMJs with 30% fewer synaptic boutons than controls.

(Sulkowski et al., 2014)

The increase in bouton number at the neuromuscular junction which is seen in third instar larvae expressing mav^{Scer\UAS.T:Avic\GFP} under the control of Scer\GAL4^Gli-rL82 is completely suppressed by gbb¹/+.

(Fuentes-Medel et al., 2012)

The neuromuscular junction expansion phenotype seen in cmpy^Δ8 mutants is partially suppressed when animals are also heterozygous for gbb¹.

(James and Broihier, 2011)

scw^gbb.PF cannot rescue the wing vein defects of gbb¹/gbb⁴ flies in a sax¹/sax² background.

(Fritsch et al., 2010)

RhoGAP92B¹/+ gbb¹/+ double heterozygous third instar larvae show a significant decrease in bouton number/muscle area and satellite bouton number at the neuromuscular junction compared to wild type.

(Nahm et al., 2010)

Only 15% of MAN1^ΔC flies heterozygous for gbb¹ show extra venation.

(Wagner et al., 2010)

In a gbb¹ heterozygous mutant, with only one copy of wild-type gbb, the absence of Dp186 through a Dys^Dp186.166.3 homozygous background is sufficient to increase synaptic currents to a level comparable to that observed in Dys^Dp186.166.3 mutants with wild-type levels of gbb expression.

Double homozygous gbb¹; Dys^Dp186.166.3 mutants display increased synaptic currents relative to gbb¹ mutants.

A gbb¹ heterozygous or homozygous background has no effect on the increase in synaptic current amplitude found upon expression of Dys^{Dp186.Scer\UAS} post-synaptically under the control of Scer\GAL4^eve.RN2.

(Fradkin et al., 2008)

spict^mut neuromuscular junction overgrowth phenotypes are fully suppressed in gbb¹/gbb⁴ mutants. The synaptic undergrowth phenotypes in larvae homozygous for spict^mut in a gbb¹/gbb⁴ background are indistinguishable from that of gbb¹/gbb⁴ mutants alone. In addition, a heterozygous gbb¹ background partially suppresses the neuromuscular junction expansion of spict^mut larvae.

(Wang et al., 2007)

gbb¹, dpp^d12/+ clones induced in the anterior of the wing leads to a greater loss of the L4-L5 intervein than gbb¹ clones but no greater loss of the L5 wing vein.

gbb¹, dpp^s4/+ clones induced in the anterior of the wing show no enhancement of the wing vein phenotypes caused by gbb¹ clones.

dpp^d5/dpp^hr56, gbb¹/+ flies show an enhancement of the dpp^d5/dpp^hr56 wing phenotype; there is an increase in the fraction of wings with L2 or L4 defects and/or a more severe reduction of the L4-L5 intervein.

(Bangi and Wharton, 2006)

Expression of rut^Scer\UAS.cZa under the control of Scer\GAL4^eve.RN2 fails to potentiate synaptic current amplitude in a gbb¹ background.

(Baines, 2004)

Dp(2;2)B16, Dp(2;2)DTD48 or Dp(2;2)B16/Dp(2;2)DTD48 cannot rescue gbb¹ homozygotes to adulthood, but there is a dramatic rescue of larval lethality to pupal/pharate adult lethality.

(Ray and Wharton, 2001)

The gbb¹/gbb⁴ phenotype is dominantly enhanced by dpp^d12; there is a greater loss of wing vein L4, wing vein L2 and the anterior crossvein than in gbb single mutant flies. There is also loss of intervein tissue, especially between veins L2 and L3 and between veins L4 and L5, resulting in a reduction in the size of the wing. A gap at the distal end of vein L3 is seen in 3% of cases. A reduction in the loss of wing vein L5 is seen in these flies. Viability is reduced. Flies show truncations and/or fusions of the distal-most tarsal segments of the male prothoracic leg. Wings derived from dpp^d6/dpp^s4 animals lack only the anterior crossvein. The anterior crossvein is restored in dpp^d6/dpp^s4 flies carrying one copy of gbb¹. The wing is reduced in size in these animals and viability is significantly reduced. Addition of Df(2L)tkv2 into gbb¹/gbb⁴ flies results in a more severe wing phenotype but less severe lethality. tkv⁴²⁷/Df(2L)tkv2 flies show slight thickening of the wing veins. This phenotype is enhanced by gbb¹. The viability of gbb¹/gbb⁴ flies is dominantly reduced by sax⁴ or sax⁵.

(Khalsa et al., 1998)

Xenogenetic Interactions

Statement

Reference

Agam\gbb1^gbb.PF and Agam\gbb2^gbb.PF each completely rescue the wing vein defects of gbb¹/gbb⁴ animals.

Agam\gbb1^gbb.PF and Agam\gbb2^gbb.PF each partially rescue the wing vein defects of gbb¹/gbb⁴ animals in a sax¹/sax² background; partial rescue of the posterior crossvein is seen and in addition loss of the distal tips of vein L5 and loss of the distal quarter of vein L4 are seen.

(Fritsch et al., 2010)

Complementation and Rescue Data

Rescued by

gbb²/gbb¹ is rescued by gbb^UAS.cKa/Scer\GAL4^Toll-6-D42

(James et al., 2014)

gbb¹ is rescued by gbb^+t6.8R

(Akiyama et al., 2012)

gbb¹ is rescued by Scer\GAL4^fat/gbb^UAS.cKa

(Ballard et al., 2010)

Partially rescued by

gbb¹ is partially rescued by gbb^t.mNS

(Akiyama et al., 2012)

gbb¹ is partially rescued by gbb^t.mS1

(Akiyama et al., 2012)

gbb²/gbb¹ is partially rescued by Scer\GAL4^BG380/gbb^UAS.cKa

(McCabe et al., 2003)

gbb²/gbb¹ is partially rescued by Scer\GAL4^G14/gbb^UAS.cKa

(McCabe et al., 2003)

gbb²/gbb¹ is partially rescued by Scer\GAL4^elav-C155/gbb^UAS.cKa

(McCabe et al., 2003)

gbb²/gbb¹ is partially rescued by gbb^UAS.cKa

(McCabe et al., 2003)

gbb⁴/gbb¹ is partially rescued by Scer\GAL4^how-24B/gbb^UAS.cKa

(Khalsa et al., 1998)

gbb⁴/gbb¹ is partially rescued by gbb^UAS.cKa/Scer\GAL4^hs.PB

(Khalsa et al., 1998)

Not rescued by

gbb¹ is not rescued by gbb^t.mNSmS1

(Akiyama et al., 2012)

Comments

Expression of gbb^Scer\UAS.cKa under the control of Scer\GAL4^Toll-6-D42 rescues the reduction in spontaneous miniature excitatory junction potential frequency, evoked excitatory junction potential amplitude and quantal content which is seen at the neuromuscular junction in gbb¹/gbb² larvae.

(James et al., 2014)

The presence of gbb^t.mNS partially rescues the lethality associated with gbb¹ mutants, with 60% of embryos surviving to adulthood. These flies exhibit defective wings.

The presence of gbb^t.mS1 partially rescues the lethality associated with gbb¹ mutants, with 7.4% of embryos surviving to adulthood. These flies exhibit defective wings. Wings from adult survivors show blistered and ectopic venation phenotypes.

(Akiyama et al., 2012)

The presence of P{UAS-gbb.K}9.9 alone (in the absence of any driver) can rescue survival of gbb¹/gbb² animals to 3rd instar or pupal stage. The additional presence of Scer\GAL4^G14 rescues bouton density and spontaneous mini-EJP (excitatory junctional potential) frequency to wild-type levels, and partially rescues spontaneous mini-EJP amplitude, evoked EJP frequency and levels of neurotransmitter release at synapses. Essentially identical results are seen when Scer\GAL4^BG380 is used instead (although bouton density not measured). However, when Scer\GAL4^elav-C155 is used there is only a slight rescue of bouton density, but the frequency and amplitude of spontaneous mini-EJPs, the amplitude of evoked EJPs and the levels of neurotransmitter release at synapses are all rescued to wild-type levels.

(McCabe et al., 2003)

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Mutant

Wild-type

Stocks (1)

Bloomington

98344

bw¹ gbb¹/SM6a

Notes on Origin

Discoverer

Comments

Homozygotes and hemizygotes over Df(2R)b23 are phenotypically indistinguishable. The gbb alleles fall into a phenotypic series. Starting with the most severe alleles: gbb¹ = gbb² > gbb³ > gbb⁴.

(Wharton et al., 1999)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (3)

Reported As

Symbol Synonym

P6-103

(Wharton et al., 1999)

gbb-60A¹

(Araujo et al., 2003, Khalsa et al., 1998)

Name Synonyms

Secondary FlyBase IDs

References (47)

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