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Allele Dmel\gbb¹

General Information
Symbol	Dmel\gbb1	Species	D. melanogaster
Name		FlyBase ID	FBal0092973
Feature type	allele	Associated gene	Dmel\gbb
Also Known As	gbb-60A1
Map ( GBrowse )
Allele class	loss of function allele, amorphic allele - genetic evidence
Mutagen
Recent Updates
Description	What does this section display? This section contains items that were added to this record for each release. It currently only tracks new links between this FlyBase report and other FlyBase data classes (e.g. genes, references, stocks) or controlled vocabulary terms (e.g. GO, anatomy terms). What does this section not display? This section does not currently display links that were removed or gene model changes.
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FB2013_03
FB2013_02
All updates	Click here to see a list of all updates to this record from FB2010_08 and on.
Nature of the Allele
Allele class	amorphic allele - genetic evidence (Wharton et al., 1999, Ray and Wharton, 2001) loss of function allele (Khalsa et al., 1998, Bangi and Wharton, 2006)
Mutagen
Mutations Mapped to the Genome
Type Location Additional Notes References point mutation 2R:19,740,390..19,740,390 comment=TGG to TGA evidence=experimental na_change=G19740390A pr_change=W371@|gbb-PA reported_na_change=G1518A reported_pr_change=W371@ (Wharton et al., 1999)
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name
UniProtKB/Swiss-Prot
UniProtKB/TrEMBL
Progenitor genotype
Nature of the lesion	Statement Reference Nucleotide substitution: G1518A. Amino acid replacement: W371@. Coordinates as in FBrf0054935. (Wharton et al., 1999)
Cytology
Phenotypic Data
Phenotypic Class
	decreased cell size | recessive | third instar larval stage (Ballard et al., 2010) developmental rate defective (with gbb4) (Ralston and Blair, 2005) female sterile (Khalsa et al., 1998) lethal (Akiyama et al., 2012) lethal (with gbb4) (Ray and Wharton, 2001) lethal | larval stage (with gbb2) (McCabe et al., 2003) lethal | larval stage | recessive (Wharton et al., 1999, Khalsa et al., 1998) lethal | recessive (Haerry et al., 1998) neuroanatomy defective (with gbb4) (McCabe et al., 2003) neurophysiology defective (Fradkin et al., 2008) neurophysiology defective (with gbb4) (McCabe et al., 2003) neurophysiology defective | recessive (Baines, 2004) small body | recessive | third instar larval stage (Ballard et al., 2010) viable (with gbb3) (Bangi and Wharton, 2006) visible (Khalsa et al., 1998) visible (with gbb4) (Ray and Wharton, 2001, Bangi and Wharton, 2006, Fritsch et al., 2010) visible | recessive (Yu et al., 2000) visible | recessive | somatic clone (Ray and Wharton, 2001) visible | recessive | third instar larval stage (Ballard et al., 2010) visible | somatic clone (Khalsa et al., 1998)
Phenotype Manifest In
	2nd posterior cell (Khalsa et al., 1998) 3rd posterior cell (Khalsa et al., 1998) anterior crossvein (Khalsa et al., 1998) anterior embryonic/larval midgut | embryonic stage (Wharton et al., 1999) bouton (with gbb2), with gbbScer\UAS.cKa (McCabe et al., 2003) bouton (with gbb4) (McCabe et al., 2003) crossvein (with gbb4) (Bangi and Wharton, 2006) crossvein | cell non-autonomous | somatic clone (Bangi and Wharton, 2006) crossvein | somatic clone (Bangi and Wharton, 2006) discal cell (Khalsa et al., 1998) dorsocentral bristle (Wharton et al., 1999) embryonic/larval brain (Khalsa et al., 1998) embryonic/larval cuticle (Wharton et al., 1999) embryonic/larval digestive system | embryonic stage (Khalsa et al., 1998) embryonic/larval fat body (Khalsa et al., 1998) embryonic/larval posterior spiracle (Wharton et al., 1999) eye (Wharton et al., 1999, Khalsa et al., 1998) fat body (Wharton et al., 1999, Ballard et al., 2010) gastric caecum (Wharton et al., 1999) imaginal disc (Wharton et al., 1999, Khalsa et al., 1998) larva (Wharton et al., 1999) leg (Khalsa et al., 1998) male germline stem cell (with gbb4) (Shivdasani and Ingham, 2003) mesothoracic bristle (Khalsa et al., 1998) metathoracic bristle (Khalsa et al., 1998) midgut constriction 1 (Wharton et al., 1999) ommatidium (Wharton et al., 1999) posterior crossvein (Haerry et al., 1998, Khalsa et al., 1998) posterior crossvein (with gbb4) (Ray and Wharton, 2001, McCabe et al., 2003) posterior crossvein | somatic clone (Ray and Wharton, 2001, Khalsa et al., 1998) postsynaptic membrane (with gbb4) (McCabe et al., 2003) scutellar bristle (Wharton et al., 1999) spermatocyte (with gbb4) (Shivdasani and Ingham, 2003) stigmatophore (Wharton et al., 1999) submarginal cell (Khalsa et al., 1998) synapse (with gbb2), with gbbScer\UAS.cKa (McCabe et al., 2003) synapse & neuromuscular junction (with gbb2), with gbbScer\UAS.cKa (McCabe et al., 2003) synaptic vesicle (with gbb4) (McCabe et al., 2003) telson (Wharton et al., 1999) testis (with gbb4) (Shivdasani and Ingham, 2003) vibrissae (Khalsa et al., 1998) wing (Khalsa et al., 1998) wing (with gbb4) (Ray and Wharton, 2001) wing | somatic clone (Ray and Wharton, 2001, Khalsa et al., 1998) wing basal cell 2 (Khalsa et al., 1998) wing cell (Khalsa et al., 1998) wing disc (with gbb3) (Ballard et al., 2010) wing margin bristle | ectopic (Khalsa et al., 1998) wing sensillum (Khalsa et al., 1998) wing vein (Yu et al., 2000, Khalsa et al., 1998) wing vein (with gbb4) (Fritsch et al., 2010) wing vein | cell non-autonomous | somatic clone (Khalsa et al., 1998) wing vein | ectopic (Khalsa et al., 1998) wing vein | ectopic | somatic clone (Khalsa et al., 1998) wing vein L2 (Khalsa et al., 1998) wing vein L3 (Khalsa et al., 1998) wing vein L3 | distal (Khalsa et al., 1998) wing vein L4 (Haerry et al., 1998) wing vein L4 | cell non-autonomous | somatic clone (Bangi and Wharton, 2006) wing vein L4 | distal (Khalsa et al., 1998) wing vein L4 | distal (with gbb4) (Ray and Wharton, 2001) wing vein L4 | somatic clone (Ray and Wharton, 2001, Khalsa et al., 1998) wing vein L5 (Haerry et al., 1998, Khalsa et al., 1998) wing vein L5 (with gbb4) (McCabe et al., 2003, Bangi and Wharton, 2006) wing vein L5 | cell non-autonomous | somatic clone (Bangi and Wharton, 2006) wing vein L5 | distal (with gbb4) (Ray and Wharton, 2001) wing vein L5 | distal | somatic clone (Ray and Wharton, 2001) wing vein L5 | somatic clone (Ray and Wharton, 2001, Khalsa et al., 1998, Bangi and Wharton, 2006)
Detailed Description
	Statement Reference Heterozygotes do not display defects in neuromuscular junction expansion. (James and Broihier, 2011) Homozygous gbb[1] 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 gbb[1] mutant larvae, however, the size of individual cells is reduced such that the entire organ is somewhat smaller in overall size. Late third instar gbb[1]/gbb[3] mutant wing imaginal discs are 50% smaller in overall area compared to the area of wild-type wing discs of the same developmental stage. gbb[1]/gbb[3] 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 gbb[1] third instar larvae have lower levels of lipids, triacylglycerides and short-chain fatty acids compared to wild-type larvae. gbb[1]/gbb[3] mutant third instar larvae have lower levels of glucose and trehalose levels than wild-type controls. gbb[1]/gbb[3] 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) gbb[1] 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 18oC 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 25oC. 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 the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
NOT Enhanced by
Statement Reference gbb1 has lethal | recessive phenotype, non-enhanceable by lilliunspecified (Su et al., 2001)
Suppressed by
Statement Reference gbb1 has lethal | recessive phenotype, suppressible | partially by Dp(2;2)B16/Dp(2;2)B16 (Ray and Wharton, 2001) gbb1 has lethal | recessive phenotype, suppressible | partially by Dp(2;2)B16/Dp(2;2)B16/Dp(2;2)DTD48 (Ray and Wharton, 2001) gbb1 has lethal | recessive phenotype, suppressible | partially by Dp(2;2)DTD48 (Ray and Wharton, 2001) gbb1 has neurophysiology defective phenotype, suppressible | partially by DysDp186.166.3 (Fradkin et al., 2008) gbb4/gbb1 has lethal phenotype, suppressible | partially by Dp(2;2)B16/Dp(2;2)B16 (Ray and Wharton, 2001) gbb4/gbb1 has lethal phenotype, suppressible | partially by Dp(2;2)B16/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 visible phenotype, suppressible by Agam\gbb1gbb.PF (Fritsch et al., 2010) gbb4/gbb1 has visible phenotype, suppressible by Agam\gbb2gbb.PF (Fritsch et al., 2010) gbb4/gbb1 has visible phenotype, suppressible by sax1/Agam\gbb1gbb.PF/sax2 (Fritsch et al., 2010) gbb4/gbb1 has visible phenotype, suppressible by sax1/Agam\gbb2gbb.PF/sax2 (Fritsch et al., 2010)
NOT suppressed by
Statement Reference gbb1 has neurophysiology defective | recessive phenotype, non-suppressible by Scer\GAL4eve.RN2/rutScer\UAS.cZa (Baines, 2004) gbb4/gbb1 has visible phenotype, non-suppressible by sax1/scwgbb.PF/sax2 (Fritsch et al., 2010)
Enhancer of
Statement Reference gbb1/gbb[+] is an enhancer of visible | dominant phenotype of sogEP7 (Araujo et al., 2003) gbb1/gbb[+] is an enhancer of visible phenotype of dppd5/dpphr56 (Bangi and Wharton, 2006) 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 neurophysiology defective phenotype of DysDp186.166.3 (Fradkin et al., 2008) gbb1/gbb[+] is a non-enhancer of visible | dominant phenotype of sogEP11 (Araujo et al., 2003) gbb1 is a non-enhancer of neurophysiology defective phenotype of DysF.Dp186.Scer\UAS, Scer\GAL4eve.RN2 (Fradkin et al., 2008)
Suppressor of
Statement Reference gbb1/gbb[+] is a suppressor | partially of neuroanatomy defective phenotype of spictmut (Wang et al., 2007) gbb1 is a suppressor of neurophysiology defective phenotype of Scer\GAL4eve.RN2, rutScer\UAS.cZa (Baines, 2004) gbb4/gbb1 is a suppressor of neuroanatomy defective phenotype of spictmut (Wang et al., 2007)
NOT Suppressor of
Statement Reference gbb1/gbb[+] is a non-suppressor of neurophysiology defective phenotype of DysDp186.166.3 (Fradkin et al., 2008) gbb1 is a non-suppressor of neurophysiology defective phenotype of DysF.Dp186.Scer\UAS, Scer\GAL4eve.RN2 (Fradkin et al., 2008)
Other
Statement Reference dpps4/dppd6, gbb1 has viable | poor phenotype (Khalsa et al., 1998) dpps4/dppd6, gbb1 has visible phenotype (Khalsa et al., 1998) gbb1, gbbScer\UAS.cKa has neurophysiology defective | heat sensitive phenotype (Baines, 2004, Baines, 2004) gbb4/gbb1, sax4 has viable | poor phenotype (Khalsa et al., 1998) gbb4/gbb1, sax5 has viable | poor phenotype (Khalsa et al., 1998) RhoGAP92B1, gbb1/gbb[+] has neuroanatomy defective | dominant | third instar larval stage phenotype (Nahm et al., 2010)
Phenotype Manifest In
Enhanced by
Statement Reference gbb1 has 2nd posterior cell phenotype, enhanceable by dppd12 (Khalsa et al., 1998) gbb1 has anterior crossvein phenotype, enhanceable by dppd12 (Khalsa et al., 1998) gbb1 has crossvein | somatic clone phenotype, enhanceable by dppd12/dpp[+] (Bangi and Wharton, 2006) gbb1 has discal cell phenotype, enhanceable by dppd12 (Khalsa et al., 1998) gbb1 has submarginal cell phenotype, enhanceable by dppd12 (Khalsa et al., 1998) gbb1 has wing basal cell 2 phenotype, enhanceable by dppd12 (Khalsa et al., 1998) gbb1 has wing cell phenotype, enhanceable by dppd12 (Khalsa et al., 1998) gbb1 has wing phenotype, enhanceable by Df(2L)tkv2 (Khalsa et al., 1998) gbb1 has wing vein L2 phenotype, enhanceable by dppd12 (Khalsa et al., 1998) gbb1 has wing vein L3 phenotype, enhanceable by dppd12 (Khalsa et al., 1998) gbb1 has wing vein L4 phenotype, enhanceable by dppd12 (Khalsa et al., 1998) gbb1 has wing vein L5 phenotype, enhanceable by dppd12 (Khalsa et al., 1998)
NOT Enhanced by
Statement Reference gbb1 has crossvein | somatic clone phenotype, non-enhanceable by dpps4/dpp[+] (Bangi and Wharton, 2006) gbb1 has wing vein L5 | somatic clone phenotype, non-enhanceable by dppd12/dpp[+] (Bangi and Wharton, 2006) gbb1 has wing vein L5 | somatic clone phenotype, non-enhanceable by dpps4/dpp[+] (Bangi and Wharton, 2006)
Suppressed by
Statement Reference gbb4/gbb1 has wing vein phenotype, suppressible by Agam\gbb1gbb.PF (Fritsch et al., 2010) gbb4/gbb1 has wing vein phenotype, suppressible by Agam\gbb2gbb.PF (Fritsch et al., 2010) gbb4/gbb1 has wing vein phenotype, suppressible by sax1/Agam\gbb1gbb.PF/sax2 (Fritsch et al., 2010) gbb4/gbb1 has wing vein phenotype, suppressible by sax1/Agam\gbb2gbb.PF/sax2 (Fritsch et al., 2010)
NOT suppressed by
Statement Reference gbb4/gbb1 has wing vein phenotype, non-suppressible by sax1/scwgbb.PF/sax2 (Fritsch et al., 2010)
Enhancer of
Statement Reference gbb1/gbb[+] is an enhancer of crossvein phenotype of dppd5/dpphr56 (Bangi and Wharton, 2006) gbb1/gbb[+] is an enhancer of wing vein L2 phenotype of dppd5/dpphr4 (Bangi and Wharton, 2006) gbb1/gbb[+] is an enhancer of wing vein L2 phenotype of dppd5/dpphr56 (Bangi and Wharton, 2006) gbb1/gbb[+] is an enhancer of wing vein phenotype of sogEP7 (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 sogEP11 (Araujo et al., 2003)
Suppressor of
Statement Reference gbb1/gbb[+] is a suppressor | partially of embryonic/larval neuromuscular junction phenotype of spictmut (Wang et al., 2007) gbb1/gbb[+] is a suppressor | partially of type I bouton | supernumerary | third instar larval stage phenotype of cmpyΔ8 (James and Broihier, 2011) gbb1/gbb[+] is a suppressor of posterior crossvein phenotype of MAN1ΔC (Wagner et al., 2010) gbb1/gbb[+] is a suppressor of wing vein | ectopic phenotype of MAN1ΔC (Wagner et al., 2010) gbb1 is a suppressor of anterior crossvein phenotype of dpps4/dppd6 (Khalsa et al., 1998) gbb4/gbb1 is a suppressor of embryonic/larval neuromuscular junction phenotype of spictmut (Wang et al., 2007)
Other
Statement Reference dppd12, gbb1 has prothoracic tarsal segment | male phenotype (Khalsa et al., 1998) dppd12, gbb4/gbb1 has prothoracic tarsal segment | male phenotype (Khalsa et al., 1998) dpps4/dppd6, gbb1 has wing phenotype (Khalsa et al., 1998) RhoGAP92B1, gbb1/gbb[+] has NMJ bouton | third instar larval stage phenotype (Nahm et al., 2010)
Additional Comments
Genetic Interactions
Statement Reference The neuromuscular junction expansion phenotype seen in cmpy[Δ8] mutants is partially suppressed when animals are also heterozygous for gbb[1]. (James and Broihier, 2011) scw[gbb.PF] cannot rescue the wing vein defects of gbb[1]/gbb[4] flies in a sax[1]/sax[2] background. (Fritsch et al., 2010) RhoGAP92B[1]/+ gbb[1]/+ 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 gbb[1] show extra venation. (Wagner et al., 2010) In a gbb[1] 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 gbb[1]; Dys[Dp186.166.3] mutants display increased synaptic currents relative to gbb[1] mutants. A gbb[1] 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) spictmut neuromuscular junction overgrowth phenotypes are fully suppressed in gbb1/gbb4 mutants. The synaptic undergrowth phenotypes in larvae homozygous for spictmut 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 spictmut larvae. (Wang et al., 2007) gbb1, dppd12/+ 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, dpps4/+ clones induced in the anterior of the wing show no enhancement of the wing vein phenotypes caused by gbb1 clones. dppd5/dpphr56, gbb1/+ flies show an enhancement of the dppd5/dpphr56 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 rutScer\UAS.cZa under the control of Scer\GAL4eve.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 dppd12; 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 dppd6/dpps4 animals lack only the anterior crossvein. The anterior crossvein is restored in dppd6/dpps4 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 gbb[1]/gbb[4] animals. Agam\gbb1[gbb.PF] and Agam\gbb2[gbb.PF] each partially rescue the wing vein defects of gbb[1]/gbb[4] animals in a sax[1]/sax[2] 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 & Rescue Data
Rescued by	gbb1 is rescued by gbb+t6.8R (Akiyama et al., 2012) gbb1 is rescued by Scer\GAL4fat/gbbScer\UAS.cKa (Ballard et al., 2010)
Partially rescued by	gbb1 is partially rescued by gbbt.mNS (Akiyama et al., 2012) gbb1 is partially rescued by gbbt.mS1 (Akiyama et al., 2012) gbb2/gbb1 is partially rescued by gbbScer\UAS.cKa/Scer\GAL4[-] (McCabe et al., 2003) gbb2/gbb1 is partially rescued by Scer\GAL4BG380/gbbScer\UAS.cKa (McCabe et al., 2003) gbb2/gbb1 is partially rescued by Scer\GAL4elav-C155/gbbScer\UAS.cKa (McCabe et al., 2003) gbb2/gbb1 is partially rescued by Scer\GAL4G14/gbbScer\UAS.cKa (McCabe et al., 2003) gbb4/gbb1 is partially rescued by gbbScer\UAS.cKa/Scer\GAL4hs.PB (Khalsa et al., 1998) gbb4/gbb1 is partially rescued by Scer\GAL4how-24B/gbbScer\UAS.cKa/Scer\GAL4how-24B (Khalsa et al., 1998)
Not rescued by	gbb1 is not rescued by gbbt.mNSmS1 (Akiyama et al., 2012)
Comments	The presence of gbb[t.mNS] partially rescues the lethality associated with gbb[1] 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 gbb[1] 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\GAL4G14 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\GAL4BG380 is used instead (although bouton density not measured). However, when Scer\GAL4elav-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)
Stocks ( 0 )
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 & Linkouts
Other Crossreferences
Linkouts
Synonyms & Secondary IDs ( 3 )
Reported As
Symbol Synonym	gbb-60A1 (Araujo et al., 2003, Khalsa et al., 1998) gbb1 (Bangi and Wharton, 2006, Christoforou et al., 2008, Baines, 2004, Wang et al., 2007, Fritsch et al., 2010, Wagner et al., 2010, Ballard et al., 2010, Fradkin et al., 2008, Akiyama et al., 2012, Pilgram et al., 2011, James and Broihier, 2011, Ball et al., 2010, Nahm et al., 2010, Quijano et al., 2011, Serpe et al., 2008) P6-103 (Wharton et al., 1999)
Name Synonym
Secondary FlyBase IDs
References ( 28 )
Generate a list of	All references relating to this allele ( 28 )
List References by type	Research paper  ( 27 ) Supplementary material  ( 1 )
Recent research papers ( 4 )
	Akiyama et al., 2012, Sci. Signal. 5(218): ra28 A Large Bioactive BMP Ligand with Distinct Signaling Properties Is Produced by Alternative Proconvertase Processing. [FBrf0217914] James and Broihier, 2011, Development 138(15): 3273--3286 Crimpy inhibits the BMP homolog Gbb in motoneurons to enable proper growth control at the Drosophila neuromuscular junction. [FBrf0214390] Pilgram et al., 2011, J. Neurosci. 31(2): 492--500 The RhoGAP crossveinless-c Interacts with Dystrophin and Is Required for Synaptic Homeostasis at the Drosophila Neuromuscular Junction. [FBrf0212767] Quijano et al., 2011, Genetics 189(3): 809--824 Wg Signaling via Zw3 and Mad Restricts Self-Renewal of Sensory Organ Precursor Cells in Drosophila. [FBrf0216675] Show all research papers ...