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General Information
D. melanogaster
FlyBase ID
Feature type
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
Nature of the Allele
Mutations Mapped to the Genome
Additional Notes

Reported as a 2 base pair deletion in codon 348, causing a frameshift.

Associated Sequence Data
DNA sequence
Protein sequence
Progenitor genotype
Nature of the lesion

A 2bp deletion that creates an early frameshift in the coding regions of both milt isoforms.

A 2bp deletion at amino acid 248 that introduces a frame shift in the coding region. This is predicted to preclude translation of two-thirds of the predicted protein.

Expression Data
Reporter Expression
Additional Information
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Modifiers Based on Experimental Evidence ( 0 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description

milt92 mutant neuronal soma have an increased mitochondrial content. These mitochondria do not display any morphology defects. Mitochondrial length is similar to controls.

The density of mitochondria (assayed by the expression of markers with a mitochondrial targeting signal) is greatly reduced in both axons and dendrites of homozygous ddaC neuron clones compared to controls. The total length of dendritic branches in the mutant neurons is not significantly affected, while the number of terminal branches is slightly reduced compared to controls.

Primary spermatocytes in homozygous germline clones induced in males appear to have normal mitochondrial morphology and distribution prior to meiosis. Onion stage spermatids derived from these spermatocytes have Nebernkerne of proper shape, which are occasionally smaller than normal and are often dissociated from nuclei (only 36% appear to be in contact with the corresponding nucleus). Unfurling of the mitochondrial derivatives from the Nebenkern does occur in mutant spermatids, but the elongation of each mitochondrial derivative is aberrant, with the two derivatives appearing to form round lobes 40% of the time at the early leaf blade stage (round lobes are not seen in wild-type cells at this stage). At later stages, the extensive surface area of the mitochondrial derivatives appears crumpled in the mutant spermatids, instead of stretched along the axoneme as in wild type, and the mitochondrial derivatives are invariably misshapen and not tightly associated pairwise as compared to wild type. In addition, the anchoring of the mitochondrial derivatives to the nucleus remains aberrant; the mitochondrial derivatives are associated end-on with the nucleus only 32% of the time (compared to 93% of the time in wild-type spermatids).

Mitochondria from milt92 germline clones associate normally with the fusome in prefollicular cysts. However, when follicles form, there is no evidence of mitochondrial transport into the oocyte and only about one-third of the normal number of mitochondria accumulate at the oocyte interior, and fail to form the Balbiani body structure usually seen. In stage 5 follicles, milt92 mutant oocytes contain fewer mitochondria than wild type, and these mitochondria remain at the anterior instead of being dispersed throughout the oocyte cytoplasm. By stage 9, mitochondria in milt92 germline clone oocytes has spread throughout the cytoplasm and reached approximately wild-type numbers.

The fusomes of milt92 cysts are indistinguishable from wild type throughout oogenesis and organelles that associate with the Balbiani body, such as Golgi elements, concentrate and move into the oocyte normally.

Mitochondria are evenly distributed in milt92 mutant follicle cells (from germ-line clones), as in wild-type follicle cells. Additionally, mitochondria from milt92 clones are clustered on the apical side of germ stem cells, as in wild type.

Axonal mitochondria are absent in milt92 larvae. This defect is selective for mitochondria.

In milt92 mutants, mitochondria are almost absent from the neuropil, indicating an absence of mitochondria at the synapse.

The axons of milt92 photoreceptors lack mitochondria.

Homozygous mutant eyes show external morphological defect. However mutants exhibit a loss of Electroretinogram on- and off-transients, indicating a synaptic transmission defect. No alteration is seen in the regular array of R7 or R8 photoreceptor axons that project into the medulla, nor are there any obvious abnormalities in the shape of the lamina. Mutant photoreceptor terminals lack mitochondria. Homozygotes, milt92/Df(2L)J-H and milt92/milt186 animals do not attain the third larval instar. These animals typically survive for 3-5 days. No animals are seen to progress before the second instar. Larvae are sluggish but exhibit robust withdrawal responses when poked. milt92 animals lacking both maternal and zygotic milt, lack mitochondria from the peripheral nerve axons and synaptic and axonal regions of the ventral ganglion.

External Data
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
NOT suppressed by
NOT Suppressor of
Additional Comments
Genetic Interactions
Xenogenetic Interactions

milt92 has no effect on the mitochondrial elongation defect seen when Hsap\MAPTR406W.Scer\UAS is expressed under the control of Scer\GAL4elav.PU, however, as in milt92 single mutants, the overall number of mitochondria is increased, with an elevated number of both elongated and normal mitochondria.

Complementation and Rescue Data
Images (0)
Stocks (0)
Notes on Origin

Isolated independently from milt186.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
References (10)