FB2025_01 , released February 20, 2025
Aberration: Dmel\Df(1)w67k30
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General Information
Symbol
Df(1)w67k30
Species
D. melanogaster
Name
FlyBase ID
FBab0001042
Feature type
chromosomal_deletion
Also Known As
Df(1)w67K30, w67k30, Dfw67k30, duf, rst
Computed Breakpoints include

3C2;3C6

Features within 3C2--3C6
Sequence coordinates
Member of large scale dataset(s)
Nature of Aberration
Cytological Order
Progenitor
Mutagen
X ray
(Eeken and Sobels, 1990, Lefevre and Green, 1972, Lefevre, 1970)
P-element activity
(Dworak et al., 2001)
Class of aberration (relative to wild type)
chromosomal_deletion
(FlyBase, 2007)
Class of aberration (relative to progenitor)
chromosomal_deletion
(Eeken and Sobels, 1990, Welshons, 1974, Lefevre and Green, 1972, Lefevre, 1971, Lefevre, 1970)
Breakpoints

3C2;3C6

(Lefevre and Green, 1972, Lefevre, 1971, Lefevre, 1970)

3C1;3C6

(Welshons, 1974)

3C1-3C2;3C6-3C7

(Eeken and Sobels, 1990)
Causes alleles
Carries alleles
Transposon Insertions
Formalized genetic data

crm << bk1 << w << su(faswb) << bk2 << N

Genetic mapping information
Comments

Deletes 5' half of the transcription unit immediately upstream of N (Kidd, Kelley and Young, 1986, Mol. Cell Biol. 6: 3094-3108)

Comments on Cytology

Deletion of 5/6 bands.

(Eeken and Sobels, 1990)

Left limit of break 1 from polytene analysis (FBrf0023492) Right limit of break 1 from inclusion of w (FBrf0023492) Limits of break 2 from polytene analysis (FBrf0023492)

Sequence Crossreferences
DDBJ / EMBL / GenBank
DNA sequence
Protein sequence
Gene Deletion and Duplication Data
Genes Deleted / Disrupted
Genes NOT Deleted / Disrupted
Complementation Data
 
Actn
(Kramers et al., 1991)
crm
(Kramers et al., 1991, Kramers et al., 1983)
crn
(Kramers et al., 1991)
dwg
(Kramers et al., 1991, Kramers et al., 1983)
egh
(Kramers et al., 1991)
gt
(Kramers et al., 1991)
kz
(Kramers et al., 1991)
l(1)2Dj
(Kramers et al., 1991)
l(1)2Dk
(Kramers et al., 1991)
l(1)2Dl
(Kramers et al., 1991)
l(1)2Dm
(Kramers et al., 1991)
l(1)2Ea
(Kramers et al., 1991)
l(1)2Ec
(Kramers et al., 1991)
l(1)2Ed
(Kramers et al., 1991)
l(1)2Fb
(Kramers et al., 1991)
l(1)2Fc
(Kramers et al., 1991)
l(1)2Fd
(Kramers et al., 1991)
l(1)2Ff
(Kramers et al., 1991)
l(1)2Fg
(Kramers et al., 1991)
l(1)3-64
(Kramers et al., 1991)
l(1)3ABa
(Kramers et al., 1991)
l(1)3ABb
(Kramers et al., 1991)
l(1)3Aj
(Kramers et al., 1991)
l(1)3Ak
(Kramers et al., 1991)
l(1)3Al
(Kramers et al., 1991)
l(1)3Am
(Kramers et al., 1991)
l(1)3An
(Kramers et al., 1991)
l(1)3Ao
(Kramers et al., 1991)
l(1)3Ap
(Kramers et al., 1991)
l(1)3Aq
(Kramers et al., 1991)
l(1)3Bb
(Kramers et al., 1991, Kramers et al., 1983)
l(1)3Bc
(Kramers et al., 1991, Kramers et al., 1983)
l(1)3Bd
(Kramers et al., 1991, Kramers et al., 1983)
l(1)3Bf
(Kramers et al., 1991, Kramers et al., 1983)
l(1)3Bg
(Kramers et al., 1991)
l(1)3Da
(Kramers et al., 1991)
l(1)3Eb
(Kramers et al., 1991)
l(1)3Ed
(Kramers et al., 1991)
l(1)7-103
(Kramers et al., 1991)
l(1)EA65
(Kramers et al., 1991)
l(1)ESHS14
(Kramers et al., 1991)
Myc
(Kramers et al., 1991)
N
(Ruiz-Gomez et al., 2000, Kramers et al., 1991, Kramers et al., 1983, Welshons, 1974)
Pgd
(Kramers et al., 1991)
Pi4KIIIα
(Kramers et al., 1991)
pn
(Kramers et al., 1991)
Raf
(Kramers et al., 1991)
sgg
(Kramers et al., 1991)
tko
(Kramers et al., 1991)
trol
(Kramers et al., 1991)
wapl
(Kramers et al., 1991)
wds
(Kramers et al., 1991)
z
(Kramers et al., 1991)
Zw10
(Kramers et al., 1991)
Molecular Data
 
Genes Duplicated
Complementation Data
Completely duplicated
Partially duplicated
Molecular Data
Completely duplicated
Partially duplicated
Genes NOT Duplicated
Complementation Data
 
Molecular Data
 
Affected Genes Inferred by Location (0)
    If no genes are listed here, it may be because the affected region is very large. The JBrowse insert above may show an error for the same reason, and other FlyBase tools such as CytoSearch may also fail for large regions. You can contact FlyBase for more help.
    In these cases, there will be no "Export to Hitlist" button to the left.
    Phenotypic Data
    In combination with other aberrations

    Mutants embryos show a lack of myoblast fusion. Gaps are seen in the visceral mesoderm. At stage 14 the gaps within the visceral band contain undifferentiated myoblasts. During further embryogenesis the midgut is surrounded by numerous unfused globular cells that cannot be assigned to either somatic or visceral myoblasts.

    (Klapper et al., 2002)

    Viable in combination with Df(1)w258-42. Viable in combination with Df(1)rst2. Lethality is rescued by Dp(1;3)wvco. Complemented by Df(1)N-81k1. Not complemented by Df(1)N-8.

    (Ruiz-Gomez et al., 2000)

    Viable in combination with Df(1)N-54l9, producing flies which have a strong vt phenotype, but are not rough eyed.

    (Lefevre, 1971)

    Male lethality can be rescued by Dp(1;3)wvco. Lethal in combination with In(1)wm4Lrst3R but not with Df(1)rst2.

    (Lefevre, 1970)

    Df(1)w67k30/Dp(1;3)wvco viable

    NOT in combination with other aberrations

    There is a complete block in myoblast attraction and fusion in the large dorsal muscle DA1 of Df(1)w67k30 mutant embryos. Mononucleate muscle founder cells (FCs) form mini muscles surrounded by several unfused fusion competent myoblasts (FCMs) with randomly oriented filopodia.

    (Bulchand et al., 2010)

    The eve-expressing DA1 founder cell undergoes no fusion in Df(1)w67k30 embryos (that lack kirre and rst).

    (Shelton et al., 2009)

    Hemizygous embryonic garland cells lack diaphragms and lacunae.

    (Weavers et al., 2009)

    Approximately 30% of garland cell nephrocytes (GCNs) remain mononucleate at early stage 16 in Df(1)w67k30 mutant embryos (in contrast to wild-type embryos where 99.6% of the GCNs are binucleate at this stage). The GCNs of stage 16 Df(1)w67k30 embryos are disorganised, misshapen and more loosely associated than in wild-type embryos.

    (Zhuang et al., 2009)

    Founder myoblasts fail to attract fusion-competent myoblasts and myoblast fusion stalls altogether - the average number of eve-positive nuclei within a DA1 muscle at stage 15 is approximately 1 compared to approximately 10 in wild type embryos.

    (Menon et al., 2005)

    The palisade of circular visceral muscle founder cells is distinctly separated from the adjacent population of fusion-competent cells in stage 13 mutant embryos, in contrast to wild type where they are closely apposed.

    (San Martin et al., 2001)

    Mutants are embryonic lethal and show no myoblast fusion.

    (Strunkelnberg et al., 2001)

    Embryos show a complete lack of fusion in the somatic mesoderm and gaps in the visceral mesoderm, whereas other mesodermal derivatives, such as fat body, gonads and heart develop normally. Myoblast fusion fails completely in Df(1)w67k30 embryos. Founder cells and fusion-competent myoblasts remain at different levels in the mesoderm, with the founders in close contact with the ectoderm, whereas the rest of the myoblasts are more internal. The myoblasts do extend filopodia, but they are randomly oriented and show no sign of being attracted preferentially toward the founders. At later stages, founder cells elongate to form mononucleate muscles that span the territory that they would have occupied as syncytia in wild-type embryos. A normal pattern of innervation by motorneurons is seen. Fusion competent myoblasts die and are eliminated by macrophages. Df(1)w67k30 embryos show an early defect in visceral mesoderm formation; instead of two bands of tightly packed visceral muscles, several gaps are seen. These gaps are not due to a reduction in the precursors, instead they might be a consequence of improper alignment or adhesion of the visceral muscles.

    (Ruiz-Gomez et al., 2000)

    Heterozygous females exhibit slightly reduced viability and fertility.

    (Eeken and Sobels, 1990)

    homozygous lethal Homozygous germline clones produce viable cells.

    (Garcia-Bellido and Robbins, 1983)

    Individuals are mutant in eye colour and texture and show the vertical bristle syndrome. Homozygous males are lethal.

    (Lefevre and Green, 1972)

    Male lethal.

    (Lefevre, 1970)

    Suppresses faswb Cell viable male lethal

    Stocks (3)
    Notes on Origin
    Discoverer

    Baker, 30th November 1967.

    (Lefevre, 1970)
     
    Balancer / Genotype Variants of the Aberration
     
    Separable Components
     
    Other Comments
     
    Synonyms and Secondary IDs (14)
    References (42)