A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Dmel\Klp67A322b24

General Information
SymbolDmel\Klp67A322b24SpeciesD. melanogaster
NameFlyBase IDFBal0183014
Feature typealleleAssociated geneDmel\Klp67A
Allele class
MutagenDelta2-3
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Description
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FB2013_03
FB2013_02
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Allele class
Mutagen
Mutations Mapped to the Genome
Type
Location
Additional Notes
References
Associated Sequence Data
DDBJ /
EMBL /
GenBank
DNA sequence
Protein sequence
Name
 
UniProtKB/Swiss-Prot
UniProtKB/TrEMBL
Progenitor genotype
Nature of the lesion
Statement
Reference
Local hopping of the P{EP} element insertion, causing a small deletion of <35bp within the promoter region of Klp67A. This causes transcription to begin at the P{EP} element instead of at the normal transcription initiation site.
Caused by insertion
Cytology
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spermatid & Nebenkern (with Df(3L)29A6)
spermatid & nucleus (with Df(3L)29A6)
spermatocyte & aster | ectopic (with Df(3L)29A6)
spermatocyte & astral microtubule (with Df(3L)29A6)
spermatocyte & centrosome | supernumerary (with Df(3L)29A6)
spermatocyte & condensed nuclear chromosome (with Df(3L)29A6)
spermatocyte & contractile ring (with Df(3L)29A6)
spermatocyte & spindle | supernumerary (with Df(3L)29A6)
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Statement
Reference
Klp67A[322b24]/Df(3L)29A6 flies are male sterile and female semi-sterile. Klp67A[322b24]/Df(3L)29A6 mutant syncytial embryos display premature mitotic spindle elongation. Klp67A[Ubi-p63E.T:Avic\GFP] restores fertility and viability to Klp67A[322b24]/Df(3L)29A6 mutants. The major mitotic defect caused by depletion of Klp67A in the mutant embryos is rescued by Klp67A[Ubi-p63E.T:Avic\GFP]. Klp67A[Ubi-p63E.T:Avic\GFP] restores wild-type spindle morphology and geometry and the dynamics of mitotic spindle poles in the rescued flies is virtually identical to that seen in wild-type embryos.
Klp67A322b24/Df(3L)29A6 mutant spermatocytes show defects throughout meiosis. In late prophase I, and to a lesser extent in late prophase II, asters ectopically localize close together in the cytoplasm, instead of at opposite sides of the nucleus. Despite this defect, the majority of primary spermatocytes assemble a bipolar spindle, form a metaphase plate and proceed through anaphase. The spindles of anaphase and metaphase I and II have astral microtubules that are longer than wild type and show abnormal chromosome segregation. In telophase I and II the astral microtubules are even longer and the central spindle is often absent or much less dense than in wild type. A minority of spermatocytes in anaphase I and II have two nuclei of different sizes. Almost half of the cells in ana-telophase II contain two spindles within the same cytoplasm, suggesting cytokinesis failure during the first meiotic division. These cells also have long astral microtubules that overlap, causing highly disorganized spindle architecture. Spermatocytes in telophase I with a normal central spindle display a regular contractile ring; those with a poorly organized central spindle appear unable to assemble a contractile ring. Klp67A322b24/Df(3L)29A6 mutant spermatids often have an unusually large nebenkern associated with two or four nuclei, consistent with a failure in meiotic cytokinesis. Additionally, some spermatids contain nuclei of irregular sizes, consistent with defects in chromosome segregation during meiosis. Some mutants have polyploid spermatocytes with four not two centrosomes, suggesting that Klp67A is involved with cytokinesis in the gonial mitoses that precede meiotic division. Blastoderm embryos from Klp67A322b24/Df(3L)29A6 mothers show abnormal spindle formation and architecture throughout mitosis. During prophase, most centrosomes do not complete migration to opposite sides of the nucleus and the period from centrosome migration to nuclear breakdown is longer than in wild-type embryos. The incomplete centrosome separation causes spindles to become distorted and banana-shaped to accommodate extended microtubules from spindle poles. In some metaphase spindles, centrosomes detach from the spindle poles. Additionally, the metaphase spindle is increased in length, whether centrosome separation is normal or not. The interval between nuclear envelope breakdown and the appearance of a central spindle is longer than wild type due to an increase in time spent in metaphase and anaphase B. Unlike in wild type, mutant spindles continue to increase in length during metaphase and pole separation occurs later in anaphase B. During telophase, most spindles are missing a normal central spindle or have a greatly reduced number of midzone microtubules, which are not organized in the typical dense lateral array seen in wild type. Following telophase, two daughter spindles can form during ensuing divisions. Despite the above defects, chromosome segregation appears to proceed as in wild type.
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Reference
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Rescued by
Comments
Klp67A[Ubi-p63E.T:Avic\GFP] restores fertility and viability to Klp67A[322b24]/Df(3L)29A6 mutants. The major mitotic defect caused by depletion of Klp67A in the mutant embryos is rescued by Klp67A[Ubi-p63E.T:Avic\GFP]. Klp67A[Ubi-p63E.T:Avic\GFP] restores wild-type spindle morphology and geometry and the dynamics of mitotic spindle poles in the rescued flies is virtually identical to that seen in wild-type embryos.
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Bloomington
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Discoverer
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hide Synonyms & Secondary IDs ( 2 )
Reported As
Symbol Synonym
Klp67A322b24
 
Klp67A332b24
Name Synonym
Secondary FlyBase IDs
hide References ( 2 )
Research paper
Wang et al., 2010, Cytoskeleton (Hoboken) 67(11): 715--728
Coupling between microtubule sliding, plus-end growth and spindle length revealed by kinesin-8 depletion. [FBrf0212142]
Gandhi et al., 2004, Mol. Biol. Cell 15(1): 121--131
The Drosophila kinesin-like protein KLP67A is essential for mitotic and male meiotic spindle assembly. [FBrf0167863]