FB2025_01 , released February 20, 2025
Allele: Dmel\Myt11
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General Information
Symbol
Dmel\Myt11
Species
D. melanogaster
Name
FlyBase ID
FBal0191423
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
myt1R6
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Allele class
Nature of the Allele
Allele class
Progenitor genotype
Cytology
Description

Nucleotide substitution: ?514. A single nucleotide deletion (corresponding to amino acid residue 173) is predicted to cause a frameshift alteration in the sequence of the protein, followed by a premature stop codon at nucleotide 689 (amino acid residue 232). This truncates the protein within the kinase domain and also deletes other conserved sequence motifs near the C-terminus of the protein.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Comment:

Position of mutation on reference sequence inferred by FlyBase curator based on author statement. Mutation is a 1 bp deletion in codon 173 which leads to a frameshift and a 232 aa long protein. GAC CGA becomes ACC GAC. Identical mutation to Myt12.

Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
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
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Modifiers Based on Experimental Evidence ( 0 )
Disease
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Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Myt11 homozygous midguts exhibit increased number of dividing cells in third instar larvae and adults.

Myt11 MARCM clones exhibit increased number of dividing cells with punctuated PH3-labeling of nuclei and increased number of cells per clone. Myt11 clones exhibit mitotic cells negative for both Delta and Prospero, suggesting, by elimination, that they are either enteroblasts or pre-enterocytes.

Myt11 homozygous guts exhibit fewer number of Pdm1-positive cells with large nuclei and Pdm1 staining is most prominent in smaller, progenitor-like cells.

Myt11 homozygote mutant BrdU-labelled spermatocytes fixed at stage S5/S6 (late G2) often show fragmented nucleoli even though the chromatin has not undergone condensation, the chromosomes of labelled mutant spermatocyte appear less condensed than in stage-matched controls but the timing of meiotic events is relatively normal. The temporal coordination between nuclear envelope breakdown and chromosome condensation is also normal as is the timing of CycA translocation in the nucleus but unlike in controls, CycA is not detectable in fusomes in stage S6 Myt11 mutant spermatocytes.

The morphology of Golgi stacks as well as their numbers in Myt11 homozygous S5/S6 spermatocytes is comparable to controls, the Golgi dynamics during meiosis is also unperturbed. However, the fusome integrity is compromised in the premeiotic G2 phase-arrested Myt11 mutant spermatocytes: the fusomes and ring canals in these spermatocytes appear disrupted and/or constricted compared to controls.

 :Myt11 homozygote mutant display highly penetrant centrosomal and meiotic spindle defects (multipolar spindle) in spermatocytes but most of the Myt11 early postmeiotic cysts appear relatively normal. The centrioles in Myt11 mutants disengage prematurely (4 instead of 2 centrioles are therefore detected in majority of S3-S6 mutants spermatocytes) and appear to be randomly distributed between the daughter cells during anaphase I, resulting in postmeiotic cells with variable numbers of centrioles.

Myt11 mutant germline stem cells divide faster than controls, and these GSCS are lost more quickly.

Viable hemizygous Myt11 mutants (over Df(3L)64D-F) exhibit bristle defects affecting the dorsal thorax, head, and eye, and are male sterile. Although Myt11/Df(3L)64D-F females are fertile, they exhibit variable maternal effect lethal embryonic phenotypes in their progeny. Myt11/Df(3L)64D-F mutants exhibit normal numbers of germline stem cells. However, they do exhibit a significant increase in secondary spermatogonial cells, relative to controls. In wild-type controls, cysts containing more than eight cells are never observed, while by contrast, approximately 30% of Myt11/Df(3L)64D-F mutant testes contain at least one 16-cell cyst, implying that the secondary spermatogonia can undergo an extra round of mitosis in Myt11/Df(3L)64D-F mutants. Approximately 10% of the mutant cysts contain twice the expected numbers of primary spermatocytes or spermatids, a phenotype never seen in controls. In both 64-cell and 128-cell Myt11/Df(3L)64D-F mutant spermatid cysts, the nuclei and nebenkern are variable and aberrant-looking, which is never seen in controls. There is a marked increase in the number of cyst cell nuclei in Myt11/Df(3L)64D-F mutants, relative to controls. In Myt11/Df(3L)64D-F mutants, the seminal vesicle is empty, which in wild-type is where mature sperm translocate to after spermatid differentiation, implying a defect in sperm maturation. Myt11/Df(3L)64D-F mutant females display a comparable number of germline stem cells as in wild-type controls. However, in contrast to wild-type, approximately 30% of germline stem cells are mitotic, exhibiting a 20-fold increase in mitotic index compared to wild-type. The mutant cystoblasts and their cystocyte descendants also have a significantly higher mitotic index than normal. Myt11/Df(3L)64D-F Myt11/Df(3L)64D-F egg chambers exhibit the same number of cells as wild-type (16 cells), indicating that ectopic germline cell divisions do not account for this defect in females. Oocyte and nurse cell differentiation appears normal in Myt11/Df(3L)64D-F mutants. Examination of germaria reveals a significant increase in the number of cysts (one- to twofold), relative to controls. Although Myt11/Df(3L)64D-F mutant cystoblasts and cystocytes are similar in size to controls, the germline stem cells appear slightly smaller.

External Data
Interactions
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Phenotypic Class
Phenotype Manifest In
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Additional Comments
Genetic Interactions
Statement
Reference

Expression of poloGD7563 under the control of Scer\GAL4bam.T:Hsim\VP16 partially suppresses the premature centriole disengagement observed in Myt11 homozygote mutant spermatocytes but has no effect on the fusome integrity defects and also does not rescue the male sterility.

Expression of Wee1Scer\UAS.P\T.T:Avic\GFP-YFP.Venus under the control of Scer\GAL4bam.T:Hsim\VP16 almost completely rescues the centriole engagement and meiotic spindle abnormalities as well as the male sterility of Myt11 homozygous mutant adults but does not restore the fusome defects.

Expression of CycAKK101548 under the control of Scer\GAL4bam.T:Hsim\VP16 in the Myt11 homozygote mutant background partially rescues the fusome defects as well as the premature centriole disengagement and multipolar meiotic spindle defects characteristic for Myt11 mutants but fails to restore the male sterility.

Expression of ruxScer\UAS.P\T.cUa under the control of Scer\GAL4bam.T:Hsim\VP16 in the Myt11 homozygote mutant background partially rescues the male sterility as well as the spermatocyte fusome defects and almost fully rescues the premature centriole disengagement and meiotic spindle defects of Myt11 mutants.

Expression of CycBKK101163 under the control of either Scer\GAL4bam.T:Hsim\VP16 or Scer\GAL4topi.T:Hsim\VP16 does not rescue the spermatocyte fusome, centriole and meiotic spindle defects characteristic for Myt11 homozygote mutant males.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

Expression of Myt1Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4bam.T:Hsim\VP16 fully rescues the fusome defects in spermatocytes and almost completely restores male fertility of Myt11 homozygous adults. Expression under the Scer\GAL4topi.T:Hsim\VP16 driver only partially rescues the fusome defects in spermatocytes and also partially restores male fertility of Myt11 homozygous adults.

The multipolar meiotic spindle defect frequently observed in spermatocytes of Myt11 homozygote mutant males is rescued by combination with Myt1βTub85D.T:Avic\GFP-EGFP.

Cell proliferation defects, including germline cysts and the adult bristle phenotype observed in Myt11/Df(3L)64D-F mutants is rescued by addition of Myt1+t3.6.

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Stocks (1)
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Synonyms and Secondary IDs (3)
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Name Synonyms
Secondary FlyBase IDs
    References (4)