FlyBase Allele Report: Dmel\Spc105R[1]

General Information

Symbol

Dmel\Spc105R¹

Species

D. melanogaster

Name

FlyBase ID

FBal0243491

Feature type

allele

Associated gene

Dmel\Spc105R

Associated Insertion(s)

Doc{}Spc105R¹

Carried in Construct

Also Known As

Spc105¹

Key Links

Allele class

amorphic allele - genetic evidence

Mutagen

Nature of the Allele

Allele class

amorphic allele - genetic evidence

(Schittenhelm et al., 2009)

Mutagen

Progenitor genotype

Associated Insertion(s)

Doc{}Spc105R¹

Cytology

Description

Insertion of an incomplete Doc element in the third exon.

(Schittenhelm et al., 2009)

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 mitotic cell cycle

(Schittenhelm et al., 2009)

abnormal mitotic cell cycle (with Df(3L)ri-XT1)

(Schittenhelm et al., 2009)

abnormal mitotic cell cycle (with Spc105R^P01511LE)

(Schittenhelm et al., 2009)

lethal | recessive

(Schittenhelm et al., 2009)

Phenotype Manifest In

Detailed Description

Statement

Reference

Mitosis 15 is slightly abnormal in Spc105R¹ embryos; lagging centromeres are often seen but the duration of mitosis 15 appears normal.

Homozygous embryos derived from heterozygous parents show defects during mitosis 16. Some cells undergo a prolonged metaphase before entering an abnormal anaphase. The remaining cells remain in prometaphase for the analysed time period (14 minutes), are unable to align their chromosomes into a metaphase plate and do not enter anaphase. More than 90% of anaphase/telophase figures are abnormal. Lagging chromosomes are seen and centromeres are rarely clustered (in contrast to wild type), and more severe defects are also seen.

Spc105R¹ embryos still have spindle assembly checkpoint function at the mitosis 16 stage (assayed by their response to colchicine treatment).

More than 90% of anaphase/telophase figures are abnormal in mitosis 16 of Spc105R¹/Df(3L)ri-XT1 and Spc105R¹/Spc105R^P01511LE embryos.

(Schittenhelm et al., 2009)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

Spc105R¹ has lethal | recessive phenotype, suppressible by Spc105R::Dwil\Spc105R^wr15

(Schittenhelm et al., 2009)

Spc105R¹ has lethal | recessive phenotype, suppressible by Spc105R::Dwil\Spc105R^wr30

(Schittenhelm et al., 2009)

Enhancer of

Statement

Reference

Spc105R[+]/Spc105R¹ is an enhancer of visible phenotype of thr^{ΔC.GMR.Tag:MYC}

(Schittenhelm et al., 2009)

Phenotype Manifest In

Enhancer of

Statement

Reference

Spc105R[+]/Spc105R¹ is an enhancer of eye phenotype of thr^{ΔC.GMR.Tag:MYC}

(Schittenhelm et al., 2009)

Additional Comments

Genetic Interactions

Statement

Reference

Xenogenetic Interactions

Statement

Reference

Spc105R::Dwil\Spc105R^wr15 and Spc105R::Dwil\Spc105R^wr30 each promote the development of Spc105R¹ hemizygotes to fertile adults.

(Schittenhelm et al., 2009)

Complementation and Rescue Data

Rescued by

Spc105R¹ is rescued by Spc105R^+tg

(Schittenhelm et al., 2009)

Spc105R¹ is rescued by Spc105R^C.EGFP

(Schittenhelm et al., 2009)

Spc105R¹ is rescued by Spc105R^wr1

(Schittenhelm et al., 2009)

Spc105R¹ is rescued by Scer\GAL4^{VP16.mat.αTub67C}/Spc105R^FL.UAS.EGFP

(Schittenhelm et al., 2009)

Partially rescued by

Spc105R¹ is partially rescued by Spc105R^C.UAS.EGFP/Scer\GAL4^{VP16.mat.αTub67C}

(Schittenhelm et al., 2009)

Spc105R^P01511LE/Spc105R¹ is partially rescued by Spc105R^wr1

(Schittenhelm et al., 2009)

Not rescued by

Spc105R¹ is not rescued by Spc105R^gC

(Schittenhelm et al., 2009)

Spc105R¹ is not rescued by Scer\GAL4^{VP16.mat.αTub67C}/Spc105R^N.UAS.EGFP

(Schittenhelm et al., 2009)

Spc105R¹ is not rescued by Spc105R^M.UAS.EGFP/Scer\GAL4^{VP16.mat.αTub67C}

(Schittenhelm et al., 2009)

Comments

Spc105R^+tg rescues both the recessive lethality and the dominant enhancement of the thr^{ΔC.GMR.T:Hsap\MYC} eye phenotype which is seen in Spc105R¹ mutants.

Spc105R^wr1 promotes the development of Spc105R¹ hemizygotes to fertile adults and almost completely rescues the abnormal anaphase/telophase figures seen during mitosis 16 in Spc105R¹/Spc105R^P01511LE embryos.

Expression of Spc105R^{FL.Scer\UAS.T:Avic\GFP-EGFP} under the control of Scer\GAL4^{mat.αTub67C.T:Hsim\VP16} rescues the mitotic defects seen in Spc105R¹ embryos at mitosis 16.

Expression of either Spc105R^{M.Scer\UAS.T:Avic\GFP-EGFP} or Spc105R^{N.Scer\UAS.T:Avic\GFP-EGFP} under the control of Scer\GAL4^{mat.αTub67C.T:Hsim\VP16} does not rescue the mitotic defects seen in Spc105R¹ embryos at mitosis 16.

Expression of Spc105R^{C.Scer\UAS.T:Avic\GFP-EGFP} under the control of Scer\GAL4^{mat.αTub67C.T:Hsim\VP16} almost completely rescues the mitotic defects seen in Spc105R¹ embryos at mitosis 16.

Spc105R^gC cannot rescue the lethality of Spc105R¹ homozygotes.

(Schittenhelm et al., 2009)

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

Separable from: Df(3R)Exel9014.

(Schittenhelm et al., 2009)

The Spc105R¹ mutation is a second site mutation that was originally discovered on the Df(3R)Exel9014 chromosome.

(Schittenhelm et al., 2009)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (2)

Reported As

Symbol Synonym

Spc105¹

(Schittenhelm et al., 2010, Schittenhelm et al., 2009)

Spc105R¹

(Das et al., 2016)

Name Synonyms

Secondary FlyBase IDs

References (3)

Report Sections

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