FlyBase Allele Report: Dmel\mys[1]

General Information

Symbol

Dmel\mys¹

Species

D. melanogaster

Name

FlyBase ID

FBal0012678

Feature type

allele

Associated gene

Dmel\mys

Associated Insertion(s)

Carried in Construct

Key Links

Allele class

amorphic allele - genetic evidence

loss of function allele

Mutagen

Nature of the Allele

Allele class

amorphic allele - genetic evidence

(Bunch et al., 1992)

loss of function allele

(Buttgereit, 1996)

Mutagen

32P

(Digan et al., 1986)

Progenitor genotype

Cytology

Polytene chromosomes normal.

Description

Deletion of at least 1kb beginning in central portion of coding region and extending towards 3' of gene, probably beyond the 3' end of the gene. Faint residual band on immunoblots (as for Df(1)C128) where product is thought to be a remnant from the maternal supply.

(Bunch et al., 1992)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

Expression Data

Reporter Expression

Additional Information

Statement

Reference

Marker for

Reflects expression of

Reporter construct used in assay

Human Disease Associations

Disease Ontology (DO) Annotations

Models Based on Experimental Evidence ( 0 )

Disease

Evidence

References

Modifiers Based on Experimental Evidence ( 0 )

Disease

Interaction

References

Comments on Models/Modifiers Based on Experimental Evidence ( 0 )

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

abnormal cell shape | P-stage | cell autonomous | somatic clone

(Walther et al., 2024)

abnormal neuroanatomy

(Stevens and Jacobs, 2002)

abnormal neuroanatomy | recessive | somatic clone

(Billuart et al., 2001)

lethal - all die during embryonic stage | recessive

(Bunch et al., 1992)

some die during embryonic stage | recessive

(Bunch et al., 1992)

Phenotype Manifest In

Detailed Description

Statement

Reference

mys¹ homozygous embryos exhibit defects in gonad niche morphogenesis compared to controls.

(Anllo et al., 2019)

mys¹ mutant class IV da neurons (generated using the MARCM system under the control of Scer\GAL4^109(2)80) show a significant increase in the amount of dendrites that cross other dendrites when analysed in a 2D plane. When these crossing overs are examined in ddaC dendrites in the apical-basal plane 88.14% are enclosed in the epidermis rather than attaching to the ECM. These dendrites are thus in different apical-basal planes and are non-contacting.

(Han et al., 2012)

Homozygous embryos have blisters and gaps in the rows of cardioblasts in the heart region of the dorsal vessel which normally align along the midline. The leading edge membrane of migrating mutant cardioblasts shows less vigorous activity than that of wild-type cardioblasts.

(Vanderploeg et al., 2012)

mys¹ mutant embryonic hemocytes do not show significant changes in the competence to undertake phagocytosis of apoptotic cells, changes in proportions of hemocytes or apoptotic cells , as compared to controls.

(Nagaosa et al., 2011)

Normal transverse tubule formation is seen in the abdominal temporary eclosion muscles of mys¹/mys^ts1 pharate adults.

(Ribeiro et al., 2011)

The somatic muscles are detached and shrunken in stage 16 homozygous embryos. These detached muscles do not show any significant apoptotic signals.

(Nguyen et al., 2007)

Embryos show weak germ band retraction and dorsal closure defects - embryos have a small dorsal hole. Those embryos that fail germ band retraction exhibit apparently normal phase I interaction, however phase II membrane apposition fails completely. Most striking is the failure of the dorsal anterior region of the amnioserosa to initiate contact with the yolk sac membrane, with subsequent high penetrance failure of dorsal closure.

(Reed et al., 2004)

The three longitudinal fascicles, as visible with Fas2, are intact in mys¹ mutants. Midline fusions of the most medial tract are seen in some segments.

(Stevens and Jacobs, 2002)

12/52 neuroblast clones in the mushroom body show obvious overextension of dorsal lobe axons. Both overextension of thin axon bundles near the tip of the dorsal lobe and overextension of a large portion of the dorsal axons is seen.

(Billuart et al., 2001)

No anti-β_PS staining at muscle attachment sites.

(Bunch et al., 1992)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

mys¹ has abnormal neuroanatomy phenotype, enhanceable by sli²

(Stevens and Jacobs, 2002)

Enhancer of

Statement

Reference

mys¹ is an enhancer of abnormal neuroanatomy phenotype of Scer\GAL4^eg-Mz360, fra^{ΔC.UAS.Tag:HA}

(O'Donnell and Bashaw, 2013)

mys¹/mys[+] is an enhancer of visible | dominant phenotype of sog^EP7

(Araujo et al., 2003)

mys¹/mys[+] is an enhancer of visible | dominant phenotype of sog^EP11

(Araujo et al., 2003)

NOT Enhancer of

Statement

Reference

mys¹/mys[+] is a non-enhancer of visible | heat sensitive phenotype of Dcr-2^UAS.cDa, Eogt^GD5084, Scer\GAL4^en.PU

(Müller et al., 2013)

mys¹/mys[+] is a non-enhancer of abnormal planar polarity phenotype of Scer\GAL4^hs.2sev, nmo^UAS.cUa

(Mirkovic et al., 2011)

mys¹ is a non-enhancer of visible phenotype of Ppt1^UAS.cKa, Scer\GAL4^GMR.PF

(Buff et al., 2007)

mys¹/mys[+] is a non-enhancer of abnormal cell polarity phenotype of Scer\GAL4^hs.2sev, shg^{dCR3h.UAS.sgGFP}

(Mirkovic and Mlodzik, 2006)

mys¹ is a non-enhancer of abnormal cell polarity phenotype of S⁰⁵⁶⁷¹

(Brown and Freeman, 2003)

Suppressor of

Statement

Reference

mys¹/mys[+] is a suppressor | partially of abnormal neuroanatomy phenotype of Scer\GAL4^elav.PLu, p130CAS^UAS.Tag:MYC

(Huang et al., 2007)

mys¹ is a suppressor of abnormal neuroanatomy phenotype of RhoGAPp190^RNAi.GAP.UAS, Scer\GAL4^ey-OK107

(Billuart et al., 2001)

NOT Suppressor of

Statement

Reference

mys¹/mys[+] is a non-suppressor of visible | heat sensitive phenotype of Dcr-2^UAS.cDa, Eogt^GD5084, Scer\GAL4^en.PU

(Müller et al., 2013)

mys¹/mys[+] is a non-suppressor of abnormal planar polarity phenotype of Scer\GAL4^hs.2sev, nmo^UAS.cUa

(Mirkovic et al., 2011)

mys¹ is a non-suppressor of visible phenotype of Ppt1^UAS.cKa, Scer\GAL4^GMR.PF

(Buff et al., 2007)

mys¹/mys[+] is a non-suppressor of abnormal cell polarity phenotype of Scer\GAL4^hs.2sev, shg^{dCR3h.UAS.sgGFP}

(Mirkovic and Mlodzik, 2006)

mys¹ is a non-suppressor of abnormal cell polarity phenotype of S⁰⁵⁶⁷¹

(Brown and Freeman, 2003)

Other

Statement

Reference

Rac1^J11/Rac1[+], mys¹ has abnormal neuroanatomy phenotype

(Soba et al., 2015)

Ret^C168/Ret[+], mys¹ has abnormal neuroanatomy phenotype

(Soba et al., 2015)

LanA^9-32, mys¹/mys[+] has abnormal neuroanatomy | third instar larval stage phenotype

(Han et al., 2012)

mys¹/mys[+], wb⁰⁹⁴³⁷ has abnormal neuroanatomy | third instar larval stage phenotype

(Han et al., 2012)

Scer\GAL4^109(2)80, mew^M6, mys¹/mys[+] has abnormal neuroanatomy | somatic clone | third instar larval stage phenotype

(Han et al., 2012)

LanB2^MB04039, mys¹/mys[+] has abnormal neuroanatomy | third instar larval stage phenotype

(Han et al., 2012)

Sema1a^UAS.cYa, mys¹/mys[+] has abnormal neuroanatomy phenotype

(Yang and Terman, 2012)

mys¹/mys[+], p130CAS¹ has partially lethal - majority die | embryonic stage phenotype

(Tikhmyanova et al., 2010)

Df(3L)Exel6083/+, mys¹ has abnormal neuroanatomy | dominant phenotype

(Huang et al., 2007)

Phenotype Manifest In

Enhanced by

Statement

Reference

mys¹ has embryonic/larval optic stalk phenotype, enhanceable by Fak^CG1/Fak56D[+]

(Murakami et al., 2007)

mys¹ has embryo | dorsal closure stage phenotype, enhanceable by Bsg^NP6293/Bsg[+]

(Reed et al., 2004)

mys¹ has fascicle phenotype, enhanceable by sli²

(Stevens and Jacobs, 2002)

Enhancer of

Statement

Reference

mys¹ is an enhancer of larval EW neuron phenotype of Scer\GAL4^eg-Mz360, fra^{ΔC.UAS.Tag:HA}

(O'Donnell and Bashaw, 2013)

mys¹ is an enhancer of symmetrical commissure phenotype of Scer\GAL4^eg-Mz360, fra^{ΔC.UAS.Tag:HA}

(O'Donnell and Bashaw, 2013)

mys¹/mys[+] is an enhancer of embryonic/larval optic stalk phenotype of Fak^CG1

(Murakami et al., 2007)

mys¹/mys[+] is an enhancer of heart primordium phenotype of sli²

(MacMullin and Jacobs, 2006)

mys¹/mys[+] is an enhancer of wing vein phenotype of sog^EP7

(Araujo et al., 2003)

mys¹/mys[+] is an enhancer of wing vein phenotype of sog^EP11

(Araujo et al., 2003)

mys¹/mys[+] is an enhancer of mitotic domain 1 | extended germ band stage phenotype of EcR^GAL4::LBD.hs

(Kozlova and Thummel, 2003)

mys¹/mys[+] is an enhancer of oocyte phenotype of Lar^5.5/Lar^13.2

(Bateman et al., 2001)

NOT Enhancer of

Statement

Reference

mys¹/mys[+] is a non-enhancer of wing blade posterior compartment | heat sensitive phenotype of Dcr-2^UAS.cDa, Eogt^GD5084, Scer\GAL4^en.PU

(Müller et al., 2013)

mys¹/mys[+] is a non-enhancer of ommatidium phenotype of Scer\GAL4^hs.2sev, nmo^UAS.cUa

(Mirkovic et al., 2011)

mys¹ is a non-enhancer of eye phenotype of Ppt1^UAS.cKa, Scer\GAL4^GMR.PF

(Buff et al., 2007)

mys¹/mys[+] is a non-enhancer of ommatidium phenotype of Scer\GAL4^hs.2sev, shg^{dCR3h.UAS.sgGFP}

(Mirkovic and Mlodzik, 2006)

mys¹ is a non-enhancer of ommatidium phenotype of S⁰⁵⁶⁷¹

(Brown and Freeman, 2003)

Suppressor of

Statement

Reference

mys¹/mys[+] is a suppressor | partially of larval intersegmental nerve phenotype of Scer\GAL4^elav.PLu, p130CAS^UAS.Tag:MYC

(Huang et al., 2007)

mys¹/mys[+] is a suppressor | partially of larval segmental nerve phenotype of Scer\GAL4^elav.PLu, p130CAS^UAS.Tag:MYC

(Huang et al., 2007)

mys¹/mys[+] is a suppressor | partially of presumptive embryonic/larval central nervous system phenotype of Scer\GAL4^elav.PLu, p130CAS^UAS.Tag:MYC

(Huang et al., 2007)

mys¹ is a suppressor of mushroom body vertical lobe phenotype of RhoGAPp190^RNAi.GAP.UAS, Scer\GAL4^ey-OK107

(Billuart et al., 2001)

NOT Suppressor of

Statement

Reference

mys¹/mys[+] is a non-suppressor of wing blade posterior compartment | heat sensitive phenotype of Dcr-2^UAS.cDa, Eogt^GD5084, Scer\GAL4^en.PU

(Müller et al., 2013)

mys¹/mys[+] is a non-suppressor of ommatidium phenotype of Scer\GAL4^hs.2sev, nmo^UAS.cUa

(Mirkovic et al., 2011)

mys¹ is a non-suppressor of eye phenotype of Ppt1^UAS.cKa, Scer\GAL4^GMR.PF

(Buff et al., 2007)

mys¹/mys[+] is a non-suppressor of ommatidium phenotype of Scer\GAL4^hs.2sev, shg^{dCR3h.UAS.sgGFP}

(Mirkovic and Mlodzik, 2006)

mys¹ is a non-suppressor of ommatidium phenotype of S⁰⁵⁶⁷¹

(Brown and Freeman, 2003)

Other

Statement

Reference

Ret^C168/Ret[+], mys¹ has larval multidendritic class IV neuron phenotype

(Soba et al., 2015)

Rac1^J11/Rac1[+], mys¹ has larval multidendritic class IV neuron phenotype

(Soba et al., 2015)

LanA^9-32, mys¹/mys[+] has larval dorsal multidendritic neuron ddaC | third instar larval stage phenotype

(Han et al., 2012)

mys¹/mys[+], wb⁰⁹⁴³⁷ has larval dorsal multidendritic neuron ddaC | third instar larval stage phenotype

(Han et al., 2012)

Scer\GAL4^109(2)80, mew^M6, mys¹/mys[+] has larval dorsal multidendritic neuron ddaC | somatic clone | third instar larval stage phenotype

(Han et al., 2012)

LanB2^MB04039, mys¹/mys[+] has larval dorsal multidendritic neuron ddaC | third instar larval stage phenotype

(Han et al., 2012)

mys¹, scb²/scb[+] has embryonic heart cardioblast phenotype

(Vanderploeg et al., 2012)

Sema1a^UAS.cYa, mys¹/mys[+] has larval intersegmental nerve branch ISNb of A1-7 phenotype

(Yang and Terman, 2012)

Sema1a^UAS.cYa, mys¹/mys[+] has larval segmental nerve branch SNa of A1-7 phenotype

(Yang and Terman, 2012)

Df(3L)Exel6083/+, mys¹ has larval intersegmental nerve phenotype

(Huang et al., 2007)

Df(3L)Exel6083/+, mys¹ has presumptive embryonic/larval central nervous system phenotype

(Huang et al., 2007)

Df(3L)Exel6083/+, mys¹ has larval segmental nerve phenotype

(Huang et al., 2007)

Additional Comments

Genetic Interactions

Statement

Reference

Ret^C168 mys¹ transheterozygous third instar larvae exhibit defects in class IV dendritic arborizing neuron dendrite crossing and a substantial loss of dendrite-ECM interaction. No phenotypes are observed in either heterozygote alone.

mys¹ Rac1^J11 transheterozygous third instar larvae exhibit defects in class IV dendritic arborizing neuron dendrite-ECM interaction. The phenotype is not observed in either heterozygote alone.

(Soba et al., 2015)

The wing blistering phenotype seen in the posterior compartment of wings in flies expressing Eogt^GD5084 under the control of Scer\GAL4^en.PU in the presence of Dcr-2^Scer\UAS.cDa is not affected if the flies are also heterozygous for mys¹.

(Müller et al., 2013)

A mys¹/Y background increases the percentage of embryonic segments displaying eg-positive axon midline crossing defects in flies expressing fra^{ΔC.Scer\UAS.T:Ivir\HA1} under the control of Scer\GAL4^eg-Mz360. However, this increase isn't considered statistically significant.

(O'Donnell and Bashaw, 2013)

22.62% of mew^M6/mys¹ mutant class IV da dendrites (generated using the MARCM system under the control of Scer\GAL4^109(2)80) are enclosed in the epidermis rather than attached to the ECM. This compares to 4.09% and 4.18% in mys¹/+ and mew^M6/+ respectively.

mew^M6/wb⁰⁹⁴³⁷ mutant third instar larvae show a mild but statistically significant increase in the proportion of dorsal midline ddaC dendrite length that is enclosed within the epidermis rather than attached to the ECM. The amount of enclosed dendrite seen in each heterozygote is similar to wild type.

mys¹/LanA^9-32 mutant third instar larvae show a mild but statistically significant increase in the proportion of dorsal midline ddaC dendritic length that is enclosed within the epidermis rather than attached to the ECM The amount of enclosed dendrite seen in each heterozygote is similar to wild type.

mys¹/LanB2^MB04039 mutant third instar larvae show a mild but statistically significant increase in the proportion of dorsal midline ddaC dendritic length that is enclosed within the epidermis rather than attached to the ECM. The amount of enclosed dendrite seen in each heterozygote is similar to wild type.

(Han et al., 2012)

mys¹/+ ; scb²/+ double heterozygous embryos show defects in continuity and alignment of the cardioblasts at the dorsal midline.

(Vanderploeg et al., 2012)

Expression of one copy of Sema-1a^Scer\UAS.cYa under the control of Scer\GAL4^how-24B in embryos that are also heterozygous for mys¹ results in axon guidance defects in the ISNb and SNa nerves, resulting in reduced muscle innervation.

(Yang and Terman, 2012)

Approximately 24% of mys¹/+; p130CAS¹/p130CAS¹ double mutants emerge as adults.

(Tikhmyanova et al., 2010)

No significant overgrowth of the neuromuscular junction is seen in Fak^N30/Fak^KG00304 third instar larvae which are also heterozygous for mys¹.

(Tsai et al., 2008)

mys¹/+ ; Df(3L)Exel6083/+ double heterozygotes show axon guidance defects characteristic of increased fasciculation in the ISNb pathway (75.4% of hemisegments), in the SNa pathway (41.8% of hemisegments) and in the central nervous system (40.0% of hemisegments). These defects are not seen in either single heterozygote.

The axon guidance defects seen in the ISNb pathway, SNa pathway and central nervous system of embryos expressing p130CAS^{Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^elav.PLu are significantly rescued by mys¹/+.

(Huang et al., 2007)

Fak56D^CG1 mys¹ double heterozygotes show more severe defects in optic stalk morphology than either single heterozygote, which each show only slight defects in optic stalk formation.

(Murakami et al., 2007)

mys¹/+; sli²/+ embryos show delayed migration of cardial cells, and clumping of heart cells.

(MacMullin and Jacobs, 2006)

A mys¹/+ background does not affect the Scer\GAL4^hs.2sev>shg^{dCR3h.Scer\UAS.T:Avic\GFP-rs} ommatidial phenotype.

(Mirkovic and Mlodzik, 2006)

Homozygous mys¹ embryos also heterozygous for Bsg^NP6293 show an enhancement of the dorsal hole phenotype seen in mys¹ embryos.

(Reed et al., 2004)

Heterozygous mys¹ has no effect on the S⁰⁵⁶⁷¹/+ ommatidial polarity phenotype.

(Brown and Freeman, 2003)

S^48-5/mys¹ mutants show 7.64%+-3.82 misrotated ommatidia compared to 9.55%+-1.43 seen in S^48-5 mutants alone.

(Gaengel and Mlodzik, 2003)

The penetrance and expressivity of the germ band retraction defect seen in embryos in which EcR^{hs.T:Scer\GAL4} is expressed using heat shock for 3 to 5 hours after egg laying is enhanced by mys¹/+.

(Kozlova and Thummel, 2003)

In mys¹/+ sli²/+ double heterozygous mutants the frequency of midline guidance errors is increased over the level observed in mys¹ homozygous mutants. Apart from midline axon crossings in one-third of the segments, the longitudinal tracts (as visible with Fas2) appear normal.

(Stevens and Jacobs, 2002)

The addition of mys¹/+ to Lar^5.5/Lar^13.2 increases the penetrance of the oocyte elongation phenotype from 14.1% to about 40%.

(Bateman et al., 2001)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Fails to complement

mys^ts3

(Bunch et al., 1992)

mys^ts1

(Bunch et al., 1992)

Comments

Approximately 5% of mys¹¹ mutant embryos expressing mys^{Ubi-p63E.T:Avic\GFP-YFP.Venus} fail to undergo germband retraction, indicating rescue.

Expression of mys^{Ubi-p63E.T:Avic\GFP-YFP.Venus} rescues the dorsal closure defects seen in mys¹¹ mutant embryos.

Expression of mys^{Ubi-p63E.T:Avic\GFP-YFP.Venus} rescues the myotendinous junction failure seen in mys¹¹ embryos.

Expression of mys^{D19A.S194A.T:Avic\GFP-EYFP.Ubi-p63E} partially rescues the germband retraction phenotype found in mys¹¹ embryos. However, the dorsal closure defects found in these embryos was not rescued and indeed in many cases appeared more severe.

The mys^{D19A.S194A.T:Avic\GFP-EYFP.Ubi-p63E} transgene confers a 22.5% rescue of myotendinous junction failure (leading to muscle attachment defects) in mid- to late-stage 17 embryos, however myotendinous junction failure is fully penetrant by early larval stages. This indicates that muscle attachment is delayed in embryos rescued with mys^{D19A.S194A.T:Avic\GFP-EYFP.Ubi-p63E}.

Expression of mys^{S196F.T:Avic\GFP-EYFP.Ubi-p63E} fails to rescue both the germband retraction and dorsal closure phenotypes found in mys¹¹ embryos.

The mys^{S196F.T:Avic\GFP-EYFP.Ubi-p63E} transgene fails to rescue the muscle detachment phenotype seen in mys¹¹ embryos, with the myotendinous junctions appearing shorter and smaller overall, compared to wild-type.

Expression of mys^{L211I.T:Avic\GFP-EYFP.Ubi-p63E} rescues both the germband retraction and dorsal closure phenotypes found in mys¹¹ embryos.

The mys^{L211I.T:Avic\GFP-EYFP.Ubi-p63E} transgene rescues the muscle detachment phenotype seen in mys¹¹ embryos.

Expression of mys^{G792N.T:Avic\GFP-EYFP.Ubi-p63E} rescues both the germband retraction and dorsal closure phenotypes found in mys¹¹ embryos.

The mys^{G792N.T:Avic\GFP-EYFP.Ubi-p63E} transgene rescues the muscle detachment phenotype seen in mys¹¹ embryos.

Expression of mys^{L796N.T:Avic\GFP-EYFP.Ubi-p63E} partially rescues the germband retraction phenotype and almost completely rescues the dorsal closure phenotype found in mys¹¹ embryos.

The mys^{L796N.T:Avic\GFP-EYFP.Ubi-p63E} transgene rescues the muscle detachment phenotype seen in mys¹¹ embryos.

Expression of mys^{804stop.T:Avic\GFP-EYFP.Ubi-p63E} partially rescues the germband retraction phenotype and fails to rescue the dorsal closure phenotype found in mys¹¹ embryos. Indeed in many cases the dorsal closure defects appear more severe.

The mys^{804stop.T:Avic\GFP-EYFP.Ubi-p63E} transgene fails to rescue the muscle detachment phenotype seen in mys¹¹ embryos, with the myotendinous junctions appearing shorter and smaller overall, compared to wild-type.

Expression of mys^{D807R.T:Avic\GFP-EYFP.Ubi-p63E} rescues both the germband retraction and dorsal closure phenotypes found in mys¹¹ embryos.

The mys^{D807R.T:Avic\GFP-EYFP.Ubi-p63E} transgene fails to rescue the muscle detachment phenotype seen in mys¹¹ embryos, with the myotendinous junctions appearing shorter and smaller overall, compared to wild-type.

Expression of mys^{Y831F.Y843F.T:Avic\GFP-EYFP.Ubi-p63E} rescues the germband retraction phenotype but exacerbates the dorsal closure phenotype found in mys¹¹ embryos.

The mys^{Y831F.Y843F.T:Avic\GFP-EYFP.Ubi-p63E} transgene rescues the muscle detachment phenotype seen in mys¹¹ embryos.

Expression of mys^{N840A.T:Avic\GFP-EYFP.Ubi-p63E} partially rescues both the germband retraction and dorsal closure phenotypes found in mys¹¹ embryos.

The mys^{N840A.T:Avic\GFP-EYFP.Ubi-p63E} transgene partially rescues the muscle detachment phenotype seen in mys¹¹ embryos. Although myotendinous junction length appears fully rescued in these animals, there is a mild but significant reduction in myotendinous area compared to wild-type.

(Pines et al., 2011)

Images (0)

Mutant

Wild-type

Stocks (3)

Bloomington

mys¹/FM4

23862

mys¹ P{neoFRT}19A/FM7c

Kyoto

105704

mys¹/FM4