FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\nanos18
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General Information
Symbol
Dmel\nanos18
Species
D. melanogaster
Name
FlyBase ID
FBal0013151
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
nosRC, nos18
Key Links
Genomic Maps

Nature of the Allele
Progenitor genotype
Cytology
Description

The splice donor site of the first intron is disrupted. Nucleotide substitution: G734A.

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

G19157973A

Comment:

The splice donor site is disrupted.

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
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
Phenotype Manifest In

cystoblast & plasma membrane

cystocyte & plasma membrane

dendritic arborising neuron & dendrite | somatic clone

female germline stem cell & plasma membrane

Detailed Description
Statement
Reference

nos18/nos53 transheterozygote third instar larvae show dendritic field coverage defects and loss of terminal branches in class IV dendritic arborizing neurons.

The majority of germaria in nos18/Df(3R)Exel6183 females produce gametes but become progressively agametic over time.

Females carrying nos18/Df(3R)nos alleles display ovaries that are largely agametic.

nos18/Df(3R)Dl-FX1 third instar larvae have a significantly higher total number of boutons at the neuromuscular junction (muscle 6/7), compared to controls; the number of active zones in type 1s boutons is also significantly increased.

From the first larval instar through the early third instar stage, class IV da neurons in nos18/Df(3R)Dl-X43 animals show no significant difference in dendrite branching complexity compared to those in control animals. Morphological defects in the class IV da neurons are first detected in nos18/Df(3R)Dl-X43 animals at the late third instar stage, when a significant reduction of higher order branching is seen compared to controls (there is a dramatic decrease in the density of terminal dendritic branches).

Late third instar nos18/nos53 larvae show a significant reduction in the density of terminal dendritic branches of the class IV da neurons.

nos18/+ females have a normal number of germline stem cells per germarium.

nos18/Df(3R)Dl-FX3 gonads in larvae at the larval/pupal transition contain many developed cysts. Homozygous germ line stem cell (GSC) clones are rapidly lost from the adult ovary; GSC loss is seen as early as 4 days after clone induction, and by the 6th or 7th day after clone induction, most ovarioles do not contain a mutant GSC.

Third larval instar class I or class II dendritic arborization neurons which are mutant for nos18 (generated using the MARCM technique) do not show an alteration in dendrite morphology, as assessed by total length of dendrites and quantitation of dendritic order. Third larval instar class III dendritic arborization neurons which are mutant for nos18 (generated using the MARCM technique) have significantly elongated dendritic spikes, but the order of dendrites and the length of major dendritic branches is indistinguishable from wild type. Third larval instar class IV dendritic arborization neurons which are mutant for nos18 (generated using the MARCM technique) show a defect in their dendrites; incomplete coverage of the epidermis is seen in about 20% of the mutant neurons (wild-type neurons cover the epidermis in a complete but non-overlapping fashion), due to a reduction of higher-order branches.

Homozygous females lay only a few eggs (an average of 6.6 eggs per week compared to 185.0 per week for control females).

Hemizygous ovaries contain only rare mature egg chambers.

Ovaries of hemizygous females or nos18/nos53 transheterozygotes contain ovarioles with either no egg chambers or 1-7 egg chambers of different stages. Some of the ovarioles produce only one egg. Ovaries with no developing germ cells occur. Mutant females show three types of egg laying pattern. TypeI (50% hemizygotes): Egg deposition begins on day 2 and stops by day 5. TypeII (41% hemizygotes): Egg deposition begins on day 2 and stops around day 5, to resume after 2 to 12 days. Type III (9% hemizygotes): No eggs are laid (ovarioles devoid of germ cells). Germline defects are age-dependent. Germaria eventually lose stem cells. Plasma membrane degenerates in stem cells and their descendents. The nuclear membrane is unaffected. Germaria from older females contain an abnormally high number of mitochondria. 20% of hemizygous or nos18/nos53 males show morphologically distinct testis defects: fewer sperm bundles with a large pool of primary spermatocytes filling most of the anterior region of the testis. Number of primary spermatocytes is increased threefold (for hemizygote) compared to wild type. The defective testis generally has fewer coils than wild type. Mutant males can be sorted into three types with respect to ability to inseminate females. TypeIII males are unable to inseminate females throughout a 4 week test period (5% of hemizygous males - testis always have germ cells, either undifferentiated primary spermatocytes, or apparently defective sperm). 90% of males show a Type II defect, 5% show a type 1 defect - all males are sterile by the third week.

The effects of loss of maternal and zygotic nos product on germ cell migration is studied in females with hb15 nosBN mutant germ line clones crossed to nos18/Df(3R)Dl-FX3 males. Germ cells are formed in the embryos indicating nos function is not required for their formation. nos activity is essential for germ cell migration, from stage 10 onwards. Following exit of the germ cells of the posterior midgut pocket, germ cells fail to migrate over the surface of the gut and instead cluster tightly together on the outer gut surface. Mutant germ cells are of varying size and often have an irregular surface. Zygotic nos expression cannot compensate for the loss of maternal nos. The few germ cells that appear to associate with the somatic embryonic gonad are unable to incorporate into the adult gonad even in the presence of a zygotically active copy of the gene. nos18/Df(3R)Dl-FX3 females lay a small number of eggs early in life but soon become completely sterile. Ovaries from females ranging from 1 to 40 days old are dissected and demonstrate sterility results from loss of germ cells from the ovary. Germline cysts rarely develop into egg chambers after the first few chambers have left the germarium. Putative germ line stem cells are present in the germaria of many mutants ovarioles for at least 10 days following eclosion, these have completely disappeared by 21 days. Transplantation of wild type germ cells can rescue the nos ovary phenotype. The transplanted cells populate the ovary more efficiently in embryos whose endogenous germ cells lack nos activity than in embryos with germ cells containing a zygotically active copy of nos.

Homozygous ovaries contain fewer developing cysts than normal. Many ovarioles consist of a germarium with one to three cysts followed by an extended stalk and one to three normal looking egg chambers. In more extreme cases, only remnants of spectrosome/fusome material can be detected in the anterior of the germarium.

Abdominal segmentation phenotype.

Homozygous embryos show mirror image duplications of posterior abdominal structures and telson structures. Defect in oogenesis so females only produce small numbers of eggs, presence of the P{nos-bcd3'UTR} construct does not rescue this defect.

maternal-effect lethal. segments, but have normal pole cells and pole plasm; no posterior activity in pole plasm. Transport or diffusion of the nos gene product from the posterior of the embryo seems to be essential for development of the wild-type abdominal pattern. Presence of the nos protein represses the activity of the gene product encoded by the hb maternal transcript in the posterior half of the embryo (Hulskamp, Schroder, Pfeifle, Jackle and Tautz, 1989; Irish, Lehmann and Akam, 1989; Struhl, 1989). Eggs deficient for both hb and nos, when fertilized by hb+ sperm, develop into normal embryos and subsequently into viable flies. Mutant embryos lack abdominal

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Suppressed by
Statement
Reference

nanos18/Df(3R)nanos has germline stem cell phenotype, suppressible by bamEP667/bam[+]

nanos18/Df(3R)nanos has ovary phenotype, suppressible by bgcn[+]/bgcnbgcnP.GFP

nanos18/Df(3R)nanos has germline stem cell phenotype, suppressible by bgcn[+]/bgcnbgcnP.GFP

nanos18/Df(3R)nanos has ovary phenotype, suppressible by bam[+]/bamBG

nanos18/Df(3R)nanos has germline stem cell phenotype, suppressible by bam[+]/bamBG

nanos18/Df(3R)nanos has ovary phenotype, suppressible by bamEP667/bam[+]

nanos18 has egg phenotype, suppressible by Hmag\nanos1nos.UTR

nanos18 has phenotype, suppressible by cup13

nanos18 has phenotype, suppressible by cup15

nanos18 has phenotype, suppressible by cup20

nanos18 has phenotype, suppressible by cup24

nanos18 has phenotype, suppressible by cup26

nanos18 has phenotype, suppressible by cup3

nanos18 has phenotype, suppressible by cup1

nanos18 has egg chamber phenotype, suppressible by cup21/cup[+]

nanos18 has egg chamber phenotype, suppressible by cup[+]/cup8

nanos18 has ovary phenotype, suppressible by cup21/cup[+]

nanos18 has ovary phenotype, suppressible by cup[+]/cup8

NOT suppressed by
Statement
Reference
Enhancer of
Statement
Reference

nanos18/nos[+] is an enhancer of female germline stem cell phenotype of twinDG24102

Suppressor of
NOT Suppressor of
Statement
Reference

nanos18/nos[+] is a non-suppressor of ovary phenotype of cupunspecified

Other
Additional Comments
Genetic Interactions
Statement
Reference

The dendritic arborization defects observed in class IV dendritic arborizing neurons of nos18/nos53 third instar larvae are suppresed by combination with a single copy of hidA206 or by expression of any of the following: DroncKK104278, DriceGD12284 or Dcp-1KK106134 under the control of Scer\GAL4477 in the mutant background.

The loss of germline stem cells seen in the ovaries of homozygous twinDG24102 females is accelerated if the females are also heterozygous for nos18.

Tumour growth is strongly suppressed in the ovaries of snf148/snf148 ; nos18/Df(3R)Exel6183 females. In young animals, 35% of germaria are agametic, In older animals the fraction of agametic germaria increases to 74%, with a marked reduction in tumour size compared with similar aged snf148/snf148 females. The majority of surviving double mutant germ cells have abnormal fusome-like structures and fail to differentiate (indicating that they are more similar to snf than nos mutant germ cells).

Ovaries of nos18/Df(3R)nos females that are also heterozygous for bamBG or bamEP667 produce many egg chambers. Removing one copy of bam increases egg chamber formation at least 10-fold in a nos18/Df(3R)nos background.

Ovaries of nos18/Df(3R)nos females that are also heterozygous for bgcnbgcnP.T:Avic\GFP produce many egg chambers. Removing this copy of bgcn increases egg chamber formation in nos18/Df(3R)nos mutants.

The phenotype of extra germline stem cells that is seen in the germarium of females expressing stwlEY05697 under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 is suppressed if the females also carry nos18/+.

The precocious differentiation of primordial germ cells which is seen in nos18/Df(3R)Dl-FX3 larval ovaries is partially suppressed by expression of dppScer\UAS.cSa or tkvQD.Scer\UAS under the control of Scer\GAL4nos.UTR.T:Hsim\VP16.

Third larval instar class I dendritic arborization neurons of third instar larvae which are mutant for both pum1 and nos18 (generated using the MARCM technique) do not have any defects in dendrite morphology. Third larval instar class III dendritic arborization neurons which are mutant for both pum1 and nos18 (generated using the MARCM technique) show an increase in the number of long dendritic spikes to a similar extent as that seen in the single mutant class III dendritic arborization neurons. Third larval instar class IV dendritic arborization neurons which are mutant for both pum1 and nos18 (generated using the MARCM technique) show incomplete innervation of the epidermal territory in about 18% of neurons, an extent similar to that seen in the single mutant class IV dendritic arborization neurons.

The oogenesis defects seen in hemizygous nos18 females are substantially suppressed by one copy of cup8 or cup21. Many egg chambers in the rescued ovaries appear normal and mature into oocytes that are fertilised and oviposited (the resulting embryos develop no abdominal segments). The rescued females lay eggs for at least 3 weeks.

Xenogenetic Interactions
Statement
Reference

Hmag\nos1nos.UTR partially rescues the egg laying defects of nos18 females. Hmag\nos1nos.UTR fails to rescue the abdominal defects of embryos derived from nos18 females.

Complementation and Rescue Data
Partially rescued by
Not rescued by
Comments
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer

Lehmann.

Comments
Comments

Strong allele of nos. Cytoplasmic transplantation of wild type plasm into the abdominal region restores normal abdominal development: surviving adults are fertile.

Cytoplasm from the posterior pole of D.pseudoobscura.pseudoobscura, D.virilis, D.hydei, M.domestica and C.samoensis embryos is injected into the abdominal region of homozygous early cleavage stage embryos. Injected embryos displayed partial or complete abdominal segmentation, the frequency of strong rescue decreases with increasing evolutionary distance of the donor.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
References (33)