Allele Dmel\nos18
| General Information | |||
|---|---|---|---|
| Symbol | Dmel\nos18 | Species | D. melanogaster |
| Name | FlyBase ID | FBal0013151 | |
| Feature type | allele | Associated gene | Dmel\nos |
| Also Known As | nosRC | ||
| Allele class | amorphic allele - genetic evidence, loss of function allele | ||
| Mutagen | ethyl methanesulfonate | ||
Recent Updates
|
|||
| Description |
What does this section display?
This section contains items that were added to this record for each release.
It currently only tracks new links between this FlyBase report and other
FlyBase data classes (e.g. genes, references, stocks) or controlled
vocabulary terms (e.g. GO, anatomy terms).
What does this section not display?
This section does not currently display links that were removed or gene model changes.
|
||
| Update Feed |
Click the icon below to subscribe to this FlyBase record and receive updates automatically through your
feed reader.
|
||
| FB2013_03 | |||
| FB2013_02 | |||
| All updates | Click here to see a list of all updates to this record from FB2010_08 and on. | ||
Nature of the Allele
| |||
| 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 The splice donor site of the first intron is disrupted. Nucleotide substitution: G734A. | ||
| Cytology | |||
Phenotypic Data
| |||
Phenotypic Class
| |||
female sterile (with Df(3R)nos) | |||
Phenotype Manifest In
| |||
cystoblast & plasma membrane cystocyte & plasma membrane dendritic arborising neuron & dendrite | somatic clone egg chamber (with nos53) female germline stem cell & plasma membrane germarium (with Df(3R)Exel6183) germline cyst (with nos53) | |||
Detailed Description
| |||
Statement Reference The majority of germaria in nos[18]/Df(3R)Exel6183 females produce gametes but become progressively agametic over time. From the first larval instar through the early third instar stage, class IV da neurons in nos[18]/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 nos[18]/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 nos[18]/nos[53] 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
| |||
| Linkouts | |||
Interactions
| |||
|
|||
Phenotypic Class
| |||
Phenotype Manifest In
| |||
Suppressed by | |||
Statement Reference nos18/Df(3R)Dl-FX3 has germline cell | female | larval stage phenotype, suppressible | partially by dppScer\UAS.cSa/Scer\GAL4nos.UTR.T:Hsim\VP16 nos18/Df(3R)Dl-FX3 has germline cell | female | larval stage phenotype, suppressible | partially by Scer\GAL4nos.UTR.T:Hsim\VP16/tkvQD.Scer\UAS nos18/Df(3R)Dl-FX3 has germline cyst | ectopic phenotype, suppressible | partially by dppScer\UAS.cSa/Scer\GAL4nos.UTR.T:Hsim\VP16 nos18/Df(3R)Dl-FX3 has germline cyst | ectopic phenotype, suppressible | partially by Scer\GAL4nos.UTR.T:Hsim\VP16/tkvQD.Scer\UAS | |||
NOT suppressed by | |||
Statement Reference | |||
Suppressor of | |||
Statement Reference nos18/nos[+] is a suppressor of female germline stem cell | supernumerary phenotype of Scer\GAL4nos.UTR.T:Hsim\VP16, stwlEY05697 | |||
NOT Suppressor of | |||
Statement Reference | |||
Other | |||
Statement Reference | |||
Additional Comments
| |||
Genetic Interactions
| |||
Statement Reference Tumour growth is strongly suppressed in the ovaries of snf[148]/snf[148] ; nos[18]/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 snf[148]/snf[148] 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 nos[18]/Df(3R)nos females that are also heterozygous for bam[BG] or bam[EP667] produce many egg chambers. Removing one copy of bam increases egg chamber formation at least 10-fold in a nos[18]/Df(3R)nos background.
Ovaries of nos[18]/Df(3R)nos females that are also heterozygous for bgcn[bgcnP.T:Avic\GFP] produce many egg chambers. Removing this copy of bgcn increases egg chamber formation in nos[18]/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 & Rescue Data
| |||
| Rescued by | |||
| Partially rescued by | nos18 is partially rescued by nos295.αTub84B.UTR.T:Ivir\HA1 | ||
| Not rescued by | nos18 is not rescued by nos3.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos6.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos18.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos19.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos108.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos111.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos122.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos139.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos153.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos154.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos165.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos183.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos197.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos204.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos212.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos243.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos246.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos253.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos254.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos258.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos263.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos264.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos272.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos273.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos277.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos286.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos505.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos506.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos512.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos516.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos517.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos520.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos524.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos526.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos538.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos539.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos549.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos554.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos558.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos560.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos565.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos568.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos579.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos581.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos585.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos587.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos592.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos594.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos595.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos599.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos607.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos614.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos620.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos623.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos626.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos627.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos635.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos641.αTub84B.UTR.T:Ivir\HA1 nos18 is not rescued by nos672.αTub84B.UTR.T:Ivir\HA1 | ||
| Comments | |||
Stocks
( 0 ) | |||
Notes on Origin
| |||
| Discoverer | Lehmann. | ||
Comments
| |||
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. Strong allele of nos. Cytoplasmic transplantation of wild type plasm into the abdominal region restores normal abdominal development: surviving adults are fertile. | |||
External Crossreferences & Linkouts
| |||
| Other Crossreferences | |||
| Linkouts | |||
Synonyms & Secondary IDs
( 2 ) | |||
| Reported As | |||
| Symbol Synonym | nos18 nosRC (Zappavigna et al., 2004, Cinnamon et al., 2004, Schaner et al., 2003, Ye et al., 2004, Mochizuki et al., 2000, Verrotti and Wharton, 2000, Arrizabalaga and Lehmann, 1999, Deshpande et al., 1999, Bhat, 1999, Styhler et al., 1998, Forbes and Lehmann, 1998, Curtis et al., 1997, Murata and Wharton, 1995, Curtis et al., 1995, Gavis and Lehmann, 1992, Lehmann and Nusslein-Volhard, 1991, Maines et al., 2007, Brechbiel and Gavis, 2008, Li et al., 2009, Harris et al., 2011) | ||
| Name Synonym | |||
| Secondary FlyBase IDs | |||
References
( 26 ) | |||
| Generate a list of | |||
| List References by type |
| ||
Recent research papers ( 2 ) | |||
| |||
Recent Updates
External Crossreferences & Linkouts