|Feature type||allele||Associated gene||Dmel\mys|
|Also Known As||mysnj42, mysnj, nj42|
|Allele class||heat sensitive loss of function allele|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
May contain regulatory mutation as lesion not found within exons or splice sites of mys.
Indistinguishable from wild type on Southern blot. Immunoblots indicate βPS protein levels are comparable to wild type (within a factor of two).
|Phenotype Manifest In|
10% of mutant males show wing blisters.
Hub cells fail to localise to the apical tip of the testis in homozygous males.
Avoidance of benzaldehyde is blunted in mutant animals compared to wild type. mys[ts1]/mys and mys[ts2]/mys flies show normal odour avoidance behaviour.
0.3% of hemizygous mutant wings show a wing blister phenotype.
mys8 larvae show a reduced olfactory response to isoamyl acetate and n-butanol, but are unaffected in their response to ethyl acetate and benzaldehyde. mys8/mysolfC-A459.1F1 flies survive and show no defect in jumping ability. They show a reduced olfactory response to isoamyl acetate but respond normally to ethyl acetate.
Some venation abnormalities are seen in homozygous mutant adults. mys8/Y flies have a low frequency of wing blisters (=<10%).
2% of hemizygous males have wing blisters.
Wing blisters are seen in approximately 5-10% of hemizygotes, and approximately 30-50% of hemizygotes have held-out wings.
Retinal development begins to break down at 55% of pupal life: one half of the R8's cell bodies have fallen though the retinal floor coming to lie underneath the cone cell plate, interrupting cone cell plate contacts. By 67% of pupal life the pigment cell feet have pulled away from the grommet extracellular membrane, opening holes around the cone cell plate. By the adult stage the retinal floor is completely disrupted. Rhabdomeres buckle. Temperature shift experiments reveal that the mys function is required during cone cell plate formation.
Wings are held out at an angle of 90o to the body, when flies are reared at 29oC.
mysxR04/mys8 flies die at 25oC but survive at 18oC, and have inflated or blistered wings and often show a gap between the pigment cell feet constituting the fenestrated membrane and the layer of pigmented subretinal cells found below the basement membrane. The viable mys8 adults have held-out wings, a phenotype which is enhanced at 29oC. mys8 males have blistered wings.
Homozygotes can survive at 18oC, but their number decreases gradually as the rearing temperature is raised to 28oC where none survive.
Homozygotes show no jumping response and severe muscular defects.
Homozygous wing is wild type in appearance but sometimes held abnormally away from the body due to severe wasting of the mesothoracic and metathoracic tergotrochanteral muscles. This phenotype is enhanced in heterozygotes. In combination with Df(1)C128 wings display morphogenetic defects, wing blisters, the formation of extra crossveins between L2 and L3 and abnormal 'delta' thickenings at vein intersections. Heterozygotes with mysxR04 are lethal. Double hemizygous and homozygous mutants with mysxR04 are lethal.
adults survive as nonjumpers
mys8/mys[+] is an enhancer of visible | female phenotype of FakScer\UAS.T:Ivir\HA1, Scer\GAL4en-e16E
|Phenotype Manifest In|
|NOT Enhanced by|
The frequency of wing blisters seen in mys/Y flies is increased to 54% if they are also expressing tnc[dsRNA.Scer\UAS.cFa] under the control of Scer\GAL4[Act5C.PI], and the overall frequency of wing defects is increased to 68%.
mys ; Lasp/+ males show a stronger hub cell mislocalisation phenotype than mys males. The double mutant males have wild-type fertility.
The penetrance of the wing blistering phenotype seen in females expressing Fak56DScer\UAS.T:Ivir\HA1 under the control of Scer\GAL4en-e16E at 25oC is increased from 28% to 44% if they are carrying mys8/+. Males expressing Fak56DScer\UAS.T:Ivir\HA1 under the control of Scer\GAL4en-e16E at 25oC and hemizygous for mys8 show 31% wing blistering (compared to 0% wing blistering in a mys+ background).
The addition of wb4Y18/+ to mys8 hemizygotes enhances the wing blister phenotype, so that 28% of wings show a blistering phenotype. The addition of LanA9-32 does not enhance this phenotype.
The addition of crol04418, crol06470 does not enhance the wing blistering phenotype of mys8/Y flies. The addition of crolk08217 does enhance the wing blistering phenotype of mys8/Y flies by 3 fold. The addition of crol3ex5 enhances the wing blistering phenotype of mys8/Y flies by about 50%. This is significantly less than the enhancement seen by crolk08217. The addition of EcRC300Y or EcRM554fs enhances the wing blistering phenotype of mys8/Y flies by about three or four-fold respectively. The amount of balloon wings is increased several fold in both cases.
The frequency of wing blisters in mys8 hemizygotes is dominantly enhanced by bsV100, cassE48, puriV4 or moaV50. The frequency of wing blisters in mys8 hemizygotes is not dominantly enhanced by pygE16, pygE50, shotV104, shotV167, takV27, takV42, aukV106, aukV162, howT1, howT90, bsV121, cassE44, puriV15, bloV99, bloV134 or moaV88. The frequency of wing blisters seen in mys11/mys8 flies is not dominantly enhanced by potP3.
The frequency of wing blisters of mys8 hemizygotes is slightly increased (to approximately 20%) if the flies are also heterozygous for aukunspecified, auk2R-4, shotunspecified, shot65-2, blounspecified, blo2R-17, kiwiunspecified, kiwi2R-3, mamunspecified or 2R-L84-2, moderately increased (to approximately 40%) if the flies are also heterozygous for bub2L-2, and strongly increased if the flies are also heterozygous for bsunspecified, rhea2 or rhea1. The frequency of the wings held-out phenotype is enhanced if the flies are also heterozygous for stckunspecified, stck3R-17, rhea1, rhea2, pio2R-16 or piounspecified. Shows a weak genetic interaction with Dlunspecified.
Individuals in combination with cnomis1 exhibit incomplete lethality, few escapers have normal wings or an extra wing vein phenotype.
|Complementation & Rescue Data|
|Fails to complement|
|Partially rescued by|
|Not rescued by|
mys8 fails to complement the isoamyl acetate olfactory response phenotype seen in mysolfC-x3, mysolfC-x5, mysolfC-x10 and mysolfC-x17.
|Stocks ( 0 )|
|Notes on Origin|
Altered PSβ protein.
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 7 )|
(Grabbe et al., 2004, Jannuzi et al., 2004, Araujo et al., 2003, Schock and Perrimon, 2003, Bateman et al., 2001, Ayyub et al., 2000, D'Avino and Thummel, 2000, Roy and VijayRaghavan, 1999, Prout et al., 1997, Longley and Ready, 1995, Miyamoto et al., 1995, Gotwals et al., 1994, Grinblat et al., 1994, Zusman et al., 1993, Brabant and Brower, 1993, Brown, 1993, Bunch et al., 1992, Wilcox et al., 1989, Lee et al., 2008, Fraichard et al., 2010, Bhandari et al., 2006)
|Secondary FlyBase IDs|
|References ( 29 )|
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|Recent research papers (0)|
|All research papers listed in FlyBase were published before 2011|
|Recent reviews (0)|
|All reviews listed in FlyBase were published before 2011|