FlyBase Allele Report: Dmel\AGO1[k08121]

General Information

Symbol

Dmel\AGO1^k08121

Species

D. melanogaster

Name

FlyBase ID

FBal0064343

Feature type

allele

Associated gene

Dmel\AGO1

Associated Insertion(s)

P{lacW}AGO1^k08121

Carried in Construct

Also Known As

l(2)k08121, AGO1⁰⁸¹²¹

Key Links

Genomic Maps

JBrowse

Allele class

loss of function allele

Mutagen

P-element activity

Nature of the Allele

Allele class

loss of function allele

(Kataoka et al., 2001)

Mutagen

P-element activity

(BDGP Project Members, 1994-1999)

Progenitor genotype

Associated Insertion(s)

P{lacW}AGO1^k08121

Cytology

Description

P{lacW} insertion 5bp downstream of the 5' end of AGO1 predicted transcript CT42236.

(Kataoka et al., 2001)

P{lacW} insertion in the third intron of the CT20708 transcript of AGO1, 4098bp downstream of the 5' end of the transcript. The insertion is also in the second intron of the CT42234 transcript of AGO1, 1689bp downstream of the 5' end of the transcript and in the first exon of the CT42236 transcript of AGO1, 5bp downstream of the 5' end of the transcript.

(Misra, 2000.8.25)

Allele components

Component

Use(s)

Inserted element

P{lacW}

enhancer trap

Encoded product / tool

lacZ

reporter enzyme

Tagged with

Tag:NLS(P)

nuclear protein localization tag

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

transposable_element_insertion_site

2R:13,953,992..13,953,992 [+]

(Lee et al., 2015, Sudhakaran et al., 2014, McCann et al., 2011, Gehrke et al., 2010, Yang et al., 2007, Grimaud et al., 2006, Okamura et al., 2004, Kataoka et al., 2001, Misra, 2000.8.25, Spradling et al., 1999, BDGP Project Members, 1994-1999)

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

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 ( 1 )

Disease

Interaction

References

exacerbates Parkinson's disease

modeled by Hsap\LRRK2^G2019S.UAS

(Gehrke et al., 2010)

modeled by Lrrk^I1915T.UAS

(Gehrke et al., 2010)

Comments on Models/Modifiers Based on Experimental Evidence ( 0 )

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

abnormal neuroanatomy

(Lee et al., 2015)

increased cell death | germline clone

(Kataoka et al., 2001)

lethal | recessive

(Spradling et al., 1999, BDGP Project Members, 1994-1999)

lethal - all die during embryonic stage | recessive

(Kataoka et al., 2001)

some die during embryonic stage | recessive

(Kataoka et al., 2001)

Phenotype Manifest In

chordotonal organ & neuron | germ-line clone

(Kataoka et al., 2001)

dendrite

(Lee et al., 2015)

denticle row 1 | germline clone (with Df(2R)50C-45)

(Kataoka et al., 2001)

embryonic/larval glial cell | germline clone

(Kataoka et al., 2001)

female germline stem cell

(Yang et al., 2007)

female germline stem cell (with AGO1¹⁴)

(Yang et al., 2007)

female germline stem cell (with AGO1^EMS)

(Yang et al., 2007)

larval longitudinal connective | germline clone

(Kataoka et al., 2001)

larval multidendritic class IV neuron

(Lee et al., 2015)

oocyte | germline clone

(Azzam et al., 2012)

presumptive embryonic/larval peripheral nervous system | germline clone

(Kataoka et al., 2001)

spermatocyte | spermatogenesis

(Bozzetti et al., 2015)

spermatocyte | spermatogenesis (with AGO1⁰⁴⁸⁴⁵)

(Bozzetti et al., 2015)

symmetrical commissure | germline clone

(Kataoka et al., 2001)

ventral denticle belt | germline clone (with Df(2R)50C-45)

(Kataoka et al., 2001)

Detailed Description

Statement

Reference

AGO1^k08121 heterozygotes and AGO1^k08121/AGO1⁰⁴⁸⁴⁵ transheterozygotes exhibit crystalline aggregates (of Stellate protein) in spermatocytes, which are absent in control spermatocytes.

AGO1^k08121 heterozygotes do not display significant changes in the length of third instar larval neuromuscular junctions, as compared to controls.

(Bozzetti et al., 2015)

AGO1^k08121 mutant result class IV dendritic arborizing neurons exhibit a reduction in mean terminal dendrite length.

(Lee et al., 2015)

Homozygous female germline clones result in variable loss of the oocyte. The frequency of egg chambers lacking an oocyte is dramatically increased at 14 days after eclosion (DAE) compared to 7 DAE. At 14 DAE, the most commonly observed developmental arrest amongst egg chambers lacking an oocyte is at 8 nurse cells. At 14 days DAE, region 2 of the germarium is smaller than normal and contains only 8-cell cysts with smaller and less branched fusomes than normal.

(Azzam et al., 2012)

Homozygous projection neuron (PN) clones show normal dendrite and axon targeting in adPN clones and in DL1 single cell projection neuron clones.

(Berdnik et al., 2008)

Heterozygous AGO1^k08121 flies show normal 1-d memory after spaced or massed training.

(Bolduc et al., 2008)

AGO1^k08121 females in which expression of AGO1^hs.PK via daily heat shock has been used to provide AGO1 function until eclosion have normal ovaries 3 days after eclosion. However, at 15 days old these flies show strong defects in germline stem cell maintenance in the germaria: only 6.3% of germaria have a normal looking structure containing two stem cells, 19.0% contain a single stem cell, 45.6% contain differentiated germ cells with branched fusomes only and 29.1% contain no germ cells at all.

AGO1^k08121/AGO1¹⁴ females in which expression of AGO1^hs.PK via daily heat shock has been used to provide AGO1 function until eclosion have normal ovaries 3 days after eclosion. However, at 15 days old these flies show strong defects in germline stem cell maintenance in the germaria: only 10.6% of germaria have a normal looking structure containing two stem cells, 23.9% contain a single stem cell, 60.1% contain differentiated germ cells with branched fusomes only and 5.3% contain no germ cells at all.

AGO1^k08121/AGO1^EMS females in which expression of AGO1^hs.PK via daily heat shock has been used to provide AGO1 function until eclosion have normal ovaries 3 days after eclosion. However, at 15 days old these flies show strong defects in germline stem cell maintenance in the germaria: only 10.3% of germaria have a normal looking structure containing two stem cells, 26.5% contain a single stem cell, 60.3% contain differentiated germ cells with branched fusomes only and 2.9% contain no germ cells at all.

Marked homozygous, AGO1^k08121/AGO1¹⁴ and AGO1^k08121/AGO1^EMS germline stem cell clones are lost from the ovary at a faster rate than marked control clones.

(Yang et al., 2007)

AGO1^k08121 zygotic mutants are less responsive than wild-type embryos to RNAi mediated by eve^dsRNA.cWa or ftz^dsRNA.cWa as assayed by phenotypes of dsRNA injected embryos. They are also less responsive to siRNA mediated RNAi, as assayed by the phenotypes of eve^dsRNA.si.cWa.

(Williams and Rubin, 2002)

Homozygous embryos have no abnormal denticle phenotype. AGO1^k08121/Df(2R)50C-45 embryos derived from homozygous AGO1^k08121 female germline clones show no obvious abnormality in segment polarity, but show a decrease in the number of denticle-forming epidermal cells, the reduction being severe in the most anterior denticle row. Embryos lacking maternal and zygotic AGO1 function show disruption of the longitudinal and commissural axons in the CNS at stages 14-16. There is a reduction in the number of neurons in the PNS, including an 80% reduction in the number of chordotonal neurons. The number of glial cells is also reduced. The number of neuroblasts and glioblasts appears normal. Stage 15 embryos contain more dying cells than normal.

(Kataoka et al., 2001)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

AGO1^k08121 has abnormal memory phenotype, enhanceable by Fmr1³/Fmr1[+]

(Bolduc et al., 2008)

Suppressed by

Statement

Reference

AGO1^k08121/AGO1[+], Fmr1³ has abnormal learning | dominant phenotype, suppressible by Fmr1^+t14

(Sudhakaran et al., 2014)

AGO1^k08121/AGO1[+], Atx2^X1 has abnormal learning | dominant phenotype, suppressible by Atx2^+t10.4

(McCann et al., 2011)

Enhancer of

Statement

Reference

AGO1^k08121/AGO1[+] is an enhancer of abnormal memory phenotype of Fmr1³

(Bolduc et al., 2008)

AGO1^k08121/AGO1[+] is an enhancer of abnormal memory phenotype of Fmr1^B55

(Bolduc et al., 2008)

AGO1^k08121/AGO1[+] is an enhancer of visible phenotype of sti^Z3-5829

(Sweeney et al., 2008)

NOT Enhancer of

Statement

Reference

AGO1^k08121/AGO1[+] is a non-enhancer of partially lethal - majority die | male phenotype of Df(1)roX2Δ, lncRNA:roX1^ex33A

(Menon and Meller, 2012)

Suppressor of

Statement

Reference

AGO1^k08121/AGO1[+] is a suppressor | partially of visible | dominant phenotype of gcm^Pyx

(Laneve et al., 2013)

AGO1^k08121/AGO1[+] is a suppressor of visible | dominant phenotype of gcm^Pyx

(Popkova et al., 2012)

AGO1^k08121/AGO1[+] is a suppressor of increased cell death phenotype of Diap1^RNAi.UAS, Scer\GAL4^GMR.PF

(Meyer et al., 2006)

NOT Suppressor of

Statement

Reference

AGO1^k08121/AGO1[+] is a non-suppressor of partially lethal - majority die | male phenotype of Df(1)roX2Δ, lncRNA:roX1^ex33A

(Menon and Meller, 2012)

Other

Statement

Reference

AGO1^k08121/AGO1[+], Fmr1³ has abnormal learning | dominant phenotype

(Sudhakaran et al., 2014)

AGO1^k08121/AGO1[+], Atx2^X1 has abnormal learning | dominant phenotype

(McCann et al., 2011)

Phenotype Manifest In

Suppressed by

Statement

Reference

AGO1^k08121 has spermatocyte | spermatogenesis phenotype, suppressible by aub^sting-1/aub[+]

(Bozzetti et al., 2015)

AGO1^k08121/AGO1[+], Atx2^X1 has antennal lobe glomerulus DM5 phenotype, suppressible by Atx2^+t10.4

(McCann et al., 2011)

AGO1^k08121/AGO1[+], Atx2^X1 has antennal lobe glomerulus V phenotype, suppressible by Atx2^+t10.4

(McCann et al., 2011)

Enhancer of

Statement

Reference

AGO1^k08121/AGO1[+] is an enhancer of eye phenotype of sti^Z3-5829

(Sweeney et al., 2008)

Suppressor of

Statement

Reference

AGO1^k08121/AGO1[+] is a suppressor | partially of macrochaeta | increased number phenotype of gcm^Pyx

(Laneve et al., 2013)

AGO1^k08121/AGO1[+] is a suppressor of chaeta | increased number phenotype of gcm^Pyx

(Popkova et al., 2012)

AGO1^k08121/AGO1[+] is a suppressor of eye phenotype of Diap1^RNAi.UAS, Scer\GAL4^GMR.PF

(Meyer et al., 2006)

Other

Statement

Reference

AGO1^k08121/AGO1[+], Atx2^X1 has antennal lobe glomerulus V phenotype

(McCann et al., 2011)

AGO1^k08121/AGO1[+], Atx2^X1 has antennal lobe glomerulus DM5 phenotype

(McCann et al., 2011)

AGO1^k08121, AGO2^51B has embryonic/first instar larval cuticle | segment polarity expression pattern phenotype

(Meyer et al., 2006)

AGO1^k08121, Dcr-1^Q1147X has embryonic/first instar larval cuticle | segment polarity expression pattern phenotype

(Meyer et al., 2006)

Additional Comments

Genetic Interactions

Statement

Reference

The crystalline aggregates observed in the spermatocytes of AGO1^k08121 heterozygotes are suppressed by aub^sting-1 heterozygosity.

AGO1^k08121, aub^sting-1 double homozygotes and AGO1^k08121, aub^HN2 double homozygotes do not display significant changes in the length of third instar larval neuromuscular junctions, as compared to controls.

(Bozzetti et al., 2015)

Fmr1^Δ50M, AGO1^k08121 double heterozygotes exhibit a complete block of the long-term habituation (LTH) normally seen when flies are exposed to either ethyl butyrate (EB) or CO[[2]]] for 4 days. LTH appears normal in either heterozygote alone. This loss of EB-evoked LTH is restored by expression of Fmr1^+t14. Short term habituation following one hour exposure to EB appears normal.

(Sudhakaran et al., 2014)

AGO1^k08121 dominantly partially suppresses the supernumerary bristle phenotype seen on the notum of gcm^Pyx heterozygotes.

(Laneve et al., 2013)

The survival of roX1^ex33A Df(1)roX2Δ adult males is not significantly altered if they are also heterozygous for AGO1^k08121.

(Menon and Meller, 2012)

AGO1^k08121, Atx2^X1 double heterozygotes exhibit a complete block of the long-term habituation (LTH) seen when flies are exposed to either ethyl butyrate (EB) or CO[[2]]] for 4 days. LTH appears normal in either heterozygote alone. This loss of EB-evoked LTH is restored by expression of Atx2^+t10.4. Short term habituation following one hour exposure to EB appears normal. LTH-associated structural plasticity is also blocked: although the V and DM5 glomeruli of Atx2^X1/+ flies show the expected growth following 4d of CO[[2]] or EB exposure, respectively, both the EB-evoked increase in DM5 volume and the CO[[2]]-induced increase in V are abolished in AGO1^k08121/+; Atx2^X1/+ double heterozygotes. These defects in structural plasticity are restored by Atx2^+t10.4.

(McCann et al., 2011)

Double mutant AGO1^k08121 AFO2⁴¹⁴ projection neuron (PN) clones show normal glomerular target selection in adPN clones and in DL1 single cell projection neuron clones.

(Berdnik et al., 2008)

Double heterozygous AGO1^k08121/+; Fmr1³/+ mutant flies show defective 1-d memory after spaced training, but not after massed training.

At relatively low concentrations of cycloheximide or puromycin, 1-d memory after spaced training is significantly ameliorated in AGO1^k08121/+; Fmr1³/+ or AGO1^k08121/+; Fmr1^B155/+ mutants (and unaffected in wild-type).

(Bolduc et al., 2008)

The sti^Z3-5829 rough eye phenotype is dominantly enhanced by AGO1^k08121.

(Sweeney et al., 2008)

The small eye phenotype of Scer\GAL4^GMR.PF>th^{dsRNA.Scer\UAS} flies is mildly suppressed by AGO1^k08121/+.

Embryos from AGO1^k08121; Dcr-1^Q1147X parents show segment polarity defects, a phenotype not seen in either single mutant.

AGO1^k08121; AGO2^51B double mutant embryos show a strong segment polarity defect.

(Meyer et al., 2006)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Complements

AGO1⁰⁴⁸⁴⁵

(Misra, 2000.8.25)

AGO1⁰⁴⁸⁴⁵

(BDGP Project Members, 1994-1999)

Fails to complement

AGO1^k16601

(BDGP Project Members, 1994-1999)

Rescued by

AGO1^k08121 is rescued by AGO1^hs.PW

(Williams and Rubin, 2002)

AGO1^k08121 is rescued by AGO1^hs.PK

(Kataoka et al., 2001)

AGO1^k08121/Df(2R)50C-45 is rescued by AGO1^hs.PK

(Kataoka et al., 2001)

Comments

Images (0)

Mutant

Wild-type

Stocks (2)

Bloomington

10772

y¹ w^67c23; P{lacW}AGO1^k08121/CyO

Kyoto

111238

y^d2 w¹¹¹⁸ P{ey-FLP.N}2 P{5xglBS-lacZ.38-1}TPN1; P{neoFRT}42D P{lacW}AGO1^k08121 /CyO y⁺

Notes on Origin

Discoverer

I. Kiss.

(BDGP Project Members, 1994-1999)

Comments

Not allelic to shot.

(Gregory and Brown, 1998)

Excision of the P{lacW} element reverts the lethality.

(Kataoka et al., 2001)

Unlike wild-type embryo extracts, AGO1^k08121 embryo extracts do not degrade mRNA when preincubated with a homologous dsRNA (tested for w and eve transcript targets). However, the rate of siRNA production from dsRNA in these extracts is identical to wild-type.

(Williams and Rubin, 2002)

Precise excision of the insertion reverts the lethal phenotype, producing viable and fertile flies.

(Yang et al., 2007)

Complements: shot^k04204. Complements: shot^k10821.

(BDGP Project Members, 1994-1999)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (7)

Reported As

Symbol Synonym

AGO1⁰⁸¹²¹

(Laneve et al., 2013, Bolduc et al., 2008)

AGO1^k08121

(Hanyu-Nakamura et al., 2019, Bozzetti et al., 2015, Lee et al., 2015, Berdnik et al., 2008, Berdnik et al., 2008, Grimaud et al., 2006)

Ago1^k08121

(Sweeney et al., 2008, Yang et al., 2007)

ago-1^k08121

(Zhang et al., 2023)

ago1^k08121

(Sudhakaran et al., 2014, Zhang and Emery, 2013, Azzam et al., 2012, Menon and Meller, 2012, McCann et al., 2011, Meyer et al., 2006)

l(2)k08121

(Pressman et al., 2012, Williams and Rubin, 2002, Kataoka et al., 2001, Misra, 2000.8.25, Spradling et al., 1999, Gregory and Brown, 1998)

l(2)k08121^k08121

(BDGP Project Members, 1994-1999)

Name Synonyms

Secondary FlyBase IDs

References (29)

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