Allele Dmel\mit(1)15¹⁶

General Information
Symbol	Dmel\mit(1)15¹⁶	Species	D. melanogaster
Name		FlyBase ID	FBal0012305
Feature type	allele	Associated gene	Dmel\mit(1)15
Also Known As	zw10^S1, l(1)zw10^S1

Allele class	amorphic allele - genetic evidence, loss of function allele
Mutagen	spontaneous
Recent Updates
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FB2013_03
FB2013_02
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Nature of the Allele
Allele class	amorphic allele - genetic evidence (Williams et al., 1992) loss of function allele (Williams and Goldberg, 1994)
Mutagen	spontaneous (Schalet, 1986, Williams et al., 1992)
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 Insertion of a 4.5-kb insertion of DNA at coordinate +1.7, judged to be a Doc element on the basis of restriction mapping. (Williams et al., 1992)
Caused by insertion	Doc{}mit(1)15¹⁶ (Williams et al., 2003, Williams et al., 1992)
Cytology
Phenotypic Data
Phenotypic Class
	cytokinesis defective \| recessive (Williams et al., 1996) lethal (Williams et al., 1992) lethal \| embryonic stage \| recessive (Williams and Goldberg, 1994) lethal \| pupal stage \| recessive (Williams et al., 1996) lethal \| recessive (Schalet, 1986) male sterile (Williams et al., 1996) meiotic cell cycle defective (Williams et al., 1996) mitotic cell cycle defective (Scaerou et al., 2001, Williams et al., 1996)
Phenotype Manifest In
	meiotic cell cycle (Savoian et al., 2000) mitotic anaphase (Scaerou et al., 2001) nuclear chromosome (Scaerou et al., 2001) nuclear chromosome \| embryonic stage \| germline clone (Williams and Goldberg, 1994) nucleus \| embryonic stage \| germline clone (Williams and Goldberg, 1994) onion stage spermatid (Williams et al., 1996) secondary spermatocyte (Savoian et al., 2000) spermatid (Williams et al., 1996) spermatocyte (Savoian et al., 2000) testis (Williams et al., 1996)
Detailed Description
	Statement Reference Mutant 3rd instar larval brains have a mitotic phenotype; 42.3% of anaphases are abnormal (showing lagging chromatids, chromatin bridges and nondisjunction) in untreated brains. Colchicine-treated mutant brains show 35.8% premature sister chromatid separation (compared to 0.96% in wild type) and have a mitotic index of 0.71 (compared to 2.44 in wild-type treated brains). (Scaerou et al., 2001) The duration of prometaphase in mutant spermatocytes is similar to that in wild-type spermatocytes. Prometaphase is not prolonged by treatment with taxol in mutant spermatocytes, in contrast to wild type. Chromosomes in mutant spermatocytes are less dynamic during early prometaphase than in wild-type spermatocytes, the rate of poleward chromosome motion is markedly reduced. The rate of anaphase poleward motion is reduced in mutant secondary spermatocytes. (Savoian et al., 2000) Transmission rate of Dp(1;f)J21A through females to progeny is 28%, mit(1)15 mutation has no effect on transmission. (Cook et al., 1997) Adult escaper males are sterile, testes are small and contain immotile sperm. Mutant onion stage spermatids vary considerably in size, indicative of chromosome missegregation during both meiotic divisions (nondisjunction during anaphase). Mistakes in chromosome behaviour are visualised by lagging chromosomes and chromatin bridges. Meiotic as well as mitotic defects are specific for events occurring either at anaphase onset or during anaphase proper. Mutation does not cause precocious sister chromatid separation (PSCS) during the first meiotic division but does affect cytokinesis (spermatids containing more than one nucleus per nebenkern). (Williams et al., 1996) Embryos derived from homozygous germline clones generally terminate development in the late syncytial blastoderm stages, although 15-25% of develop to later stages of embryogenesis, and 1% hatch into larvae. Mitotic synchrony is lost in embryos derived from homozygous germline clones. Chromatin bridges between nuclei, unequal segregation of chromosomes and lagging chromatids are seen at anaphase. (Williams and Goldberg, 1994) Brain cells are hyperploid. Aneuploidy involves improper chromosome segregation at anaphase: precocious sister chromatid separation. Mitotic index and the ratio of numbers of cells in anaphase to the total number of mitotic figures in larval brains is similar in wild type. (Williams et al., 1992)
External Data
Linkouts
Interactions
Phenotypic Class
NOT Enhanced by
Statement Reference mit(1)15¹⁶ has mitotic cell cycle defective phenotype, non-enhanceable by rod^X-5 (Scaerou et al., 2001)
NOT suppressed by
Statement Reference mit(1)15¹⁶ has mitotic cell cycle defective phenotype, non-suppressible by rod^X-5 (Scaerou et al., 2001)
NOT Enhancer of
Statement Reference mit(1)15¹⁶ is a non-enhancer of mitotic cell cycle defective phenotype of rod^X-5 (Scaerou et al., 2001)
NOT Suppressor of
Statement Reference mit(1)15¹⁶ is a non-suppressor of mitotic cell cycle defective phenotype of rod^X-5 (Scaerou et al., 2001)
Phenotype Manifest In
NOT Enhanced by
Statement Reference mit(1)15¹⁶ has mitotic anaphase phenotype, non-enhanceable by rod^X-5 (Scaerou et al., 2001) mit(1)15¹⁶ has nuclear chromosome phenotype, non-enhanceable by rod^X-5 (Scaerou et al., 2001)
NOT suppressed by
Statement Reference mit(1)15¹⁶ has mitotic anaphase phenotype, non-suppressible by rod^X-5 (Scaerou et al., 2001) mit(1)15¹⁶ has nuclear chromosome phenotype, non-suppressible by rod^X-5 (Scaerou et al., 2001)
NOT Enhancer of
Statement Reference mit(1)15¹⁶ is a non-enhancer of mitotic anaphase phenotype of rod^X-5 (Scaerou et al., 2001) mit(1)15¹⁶ is a non-enhancer of nuclear chromosome phenotype of rod^X-5 (Scaerou et al., 2001)
NOT Suppressor of
Statement Reference mit(1)15¹⁶ is a non-suppressor of mitotic anaphase phenotype of rod^X-5 (Scaerou et al., 2001) mit(1)15¹⁶ is a non-suppressor of nuclear chromosome phenotype of rod^X-5 (Scaerou et al., 2001)
Additional Comments
Genetic Interactions
Statement Reference Abnormal anaphases and premature sister chromatid separation occur at the same frequency in mit(1)15¹⁶ rod^X-5 double mutants as in either single mutant alone. There is no additive effect; the range of defects is quantitatively and qualitatively comparable with that for either single mutant. (Scaerou et al., 2001)
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Rescued by	mit(1)15¹⁶ is rescued by mit(1)15^+t4.6 (Williams et al., 1992)
Comments	Lethal phenotype can be rescued by P element mediated transformation of a wild type mit(1)15 gene copy. (Williams et al., 1992)
Stocks ( 0 )

Notes on Origin
Discoverer	Schalet.

External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 4 )
Reported As
Symbol Synonym	l(1)6-99 (Schalet, 1986, ) l(1)zw10^S1 (Cook et al., 1997, Williams et al., 1992, ) mit(1)15¹⁶ zw10^S1 (Williams et al., 2003, Savoian et al., 2000, Scaerou et al., 2001, Basu et al., 1999, Starr et al., 1998, Williams et al., 1996, Williams and Goldberg, 1994, Wainman et al., 2009)
Name Synonym
Secondary FlyBase IDs

References ( 11 )
Research paper	Wainman et al., 2009, J. Cell Sci. 122(11): 1747--1758 Roles of the Drosophila NudE protein in kinetochore function and centrosome migration. [FBrf0207980] Williams et al., 2003, Mol. Biol. Cell 14(4): 1379--1391 Zwilch, a new component of the ZW10/ROD complex required for kinetochore functions. [FBrf0159187] Scaerou et al., 2001, J. Cell Sci. 114(17): 3103--3114 The ZW10 and Rough Deal checkpoint proteins function together in a large, evolutionarily conserved complex targeted to the kinetochore. [FBrf0139719] Savoian et al., 2000, Nat. Cell Biol. 2(12): 948--952 The rate of poleward chromosome motion is attenuated in Drosophila zw10 and rod mutants. [FBrf0132421] Basu et al., 1999, J. Cell Biol. 146(1): 13--28 Mutations in the essential spindle checkpoint gene bub1 cause chromosome missegregation and fail to block apoptosis in Drosophila. [FBrf0109303] Starr et al., 1998, J. Cell Biol. 142(3): 763--774 ZW10 helps recruit dynactin and dynein to the kinetochore. [FBrf0104517] Cook et al., 1997, Genetics 145(3): 737--747 Identification of trans-acting genes necessary for centromere function in Drosophila melanogaster using centromere-defective minichromosomes. [FBrf0092503] Williams et al., 1996, J. Cell Biol. 134(5): 1127--1140 Bipolar spindle attachments affect redistributions of ZW10, a Drosophila centromere kinetochore component required for accurate chromosome segregation. [FBrf0090857] Williams and Goldberg, 1994, J. Cell Sci. 107(4): 785--798 Determinants of Drosophila zw10 protein localization and function. [FBrf0076726] Williams et al., 1992, J. Cell Biol. 118(4): 759--773 The Drosophila l(1)zw10 gene product, required for accurate mitotic chromosome segregation, is redistributed at anaphase onset. [FBrf0056449] Schalet, 1986, Mutat. Res. 163: 115--144 The distribution of and complementation relationships between spontaneous X-linked recessive lethal mutations recovered from crossing long-term laboratory stocks of Drosophila melanogaster. [FBrf0045066]

Allele Dmel\mit(1)1516

Allele Dmel\mit(1)15¹⁶