FlyBase Allele Report: Dmel\pAbp[k10109]

(Fingerhut et al., 2019, Chartier et al., 2015, Vazquez-Pianzola et al., 2011, Pertceva et al., 2010, Blagden et al., 2009, Sofola et al., 2007, Sigrist et al., 2003, Sigrist et al., 2000, 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 ( 0 )

Disease

Interaction

References

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

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

abnormal cell growth | dominant

(Roy et al., 2004)

abnormal cytokinesis (with pAbp^EY11561)

(Pertceva et al., 2010)

abnormal locomotor behavior | heat sensitive

(Sigrist et al., 2003)

abnormal meiotic cell cycle (with pAbp^EP310)

(Blagden et al., 2009)

abnormal neuroanatomy

(Sigrist et al., 2000)

abnormal neuroanatomy | larval stage

(Sigrist et al., 2002)

abnormal neurophysiology

(Sigrist et al., 2000)

abnormal neurophysiology | dominant

(Reiff et al., 2002)

abnormal neurophysiology | larval stage

(Sigrist et al., 2002)

female sterile | germline clone

(Vazquez-Pianzola et al., 2011)

lethal | recessive

(Vazquez-Pianzola et al., 2011, Spradling et al., 1999, BDGP Project Members, 1994-1999)

lethal - all die during embryonic stage (with Df(2R)Pcl7B)

(Blagden et al., 2009, Sigrist et al., 2000)

male sterile (with pAbp^EP310)

(Blagden et al., 2009)

some die during embryonic stage (with Df(2R)Pcl7B)

(Blagden et al., 2009, Sigrist et al., 2000)

visible | dominant

(Roy et al., 2004)

Phenotype Manifest In

bouton

(Sigrist et al., 2000)

bouton | increased number

(Reiff et al., 2002)

elongation stage spermatid (with pAbp^EY11561)

(Pertceva et al., 2010)

embryonic/larval neuromuscular junction

(Sigrist et al., 2003, Reiff et al., 2002)

mitochondrion (with pAbp^EY11561)

(Pertceva et al., 2010)

Nebenkern (with pAbp^5-SZ-4029)

(Blagden et al., 2009)

Nebenkern (with pAbp^EY11561)

(Pertceva et al., 2010)

neuromuscular junction

(Sigrist et al., 2000)

neuromuscular junction | larval stage

(Sigrist et al., 2002)

NMJ bouton | larval stage

(Sigrist et al., 2002)

nucleus (with pAbp^EY11561)

(Pertceva et al., 2010)

onion stage spermatid (with pAbp^5-SZ-4029)

(Blagden et al., 2009)

onion stage spermatid (with pAbp^EY11561)

(Pertceva et al., 2010)

oocyte | germline clone | oogenesis stage S5

(Vazquez-Pianzola et al., 2011)

oocyte | germline clone | oogenesis stage S6

(Vazquez-Pianzola et al., 2011)

spindle & spermatocyte (with pAbp^EP310)

(Blagden et al., 2009)

wing

(Roy et al., 2004)

Detailed Description

Statement

Reference

Homo- or hemizygous pAbp^k10109 is zygotic lethal.

In pAbp^k10109 mutant germline clones oogenesis does not proceed further than stages 5-6. pAbp^k10109 mutant germline clones show a variety of phenotypes in stages 5-6. These include small oocytes, mispositioned oocytes, packaging defects producing egg chambers with supernumerary nurse cells and two oocytes, polytene nurse cells and multilayered follicle cells. Some of these phenotypes may also be due to lack of pAbp in the follicle cells.

(Vazquez-Pianzola et al., 2011)

pAbp^k10109/pAbp^EY11561 heterozygotes exhibit abnormalities in spermatogenesis. these include absence of meiotic cytokinesis (in 5% of cases), resulting in formation of polyploid spermatids and defects in spermatid elongation (in approximately 100% of cases). Nuclei fail to elongate, keep a round shape and are dispersed along the cyst instead of grouping at the head of the cyst. Nebenkern DAPi staining (for DNA) appears to be non-uniform in these mutants, reflecting the effect of the trans-heterozygous mutants on mitochondrial DNA organization in at least 60% of cases. There appears to be no difference between the trans-heterozygous mutant and controls, showing that mutant mitochondrial membranes keep their integrity, but in the mutant, the onion-stage Nebenkern looks larger than in controls, and its morphology differs from a perfect sphere. Examination with an electron microscope reveals abnormal mitochondrial membranes at onion-stage spermatids in the trans-heterozygous mutant. These mitochondria also exhibit defective attachment to axonemes in the elongating spermatids.

(Pertceva et al., 2010)

pAbp^5-SZ-4029/pAbp^k10109 cysts in the testis sometimes contain spermatids with nuclei and Nebenkern that are twice the size of the surrounding spermatids. Cytokinesis is also affected, resulting in spermatids with a 2:1 and 3:1 ratio of nuclei:Nebenkern (in contrast to the wild-type ratio of 1:1 ).

18% of pAbp^EP310/pAbp^k10109 spermatocytes show defects in meiosis, with the most common phenotype being detachment of the meiotic spindles from astral microtubules.

(Blagden et al., 2009)

The rough eye phenotype observed in Fmr1^sev.PW flies is suppressed in a pAbp^k10109/+ background.

(Cziko et al., 2009)

Files heterozygous for pAbp^k10109 show wing size reduction.

(Roy et al., 2004)

pAbp^k10109 mutant larvae have significantly larger NMJs than wild type with more boutons. This effect becomes more prominent when larvae are raised at 25 or 29^oC. At 18^oC, pAbp^k10109 mutants show increased stride-frequency and locomotor speed compared to wild type, but unaltered stride-length and crawling distance. However, at 29^oC, the mutants exhibit similar locomotor parameters to wild type. There is also a greater increase in the amount of large subsynaptic eIF-4E aggregates at 29^oC, compared to wild type.

(Sigrist et al., 2003)

pAbp^k10109/+ mutants have larger evoked postsynaptic currents and significantly more boutons compared to wild type. These mutants also have proportionally larger NMJs, as is typical in animals with genetically strengthened signal transmission and unaltered muscle input resistance. As the boutons of these mutants show normal levels of Ca²⁺ signalling, it appears that the raised levels of released presynaptic vesicles may be due to the large numbers of contributing boutons. The large NMJs, which contain a larger total number of T-bars than wild-type boutons, continue to transmit without significant derepression at stimulation frequencies that cause considerable depression of signal transmission in wild-type NMJs.

(Reiff et al., 2002)

pAbp^k10109/+ mutants exhibit a significant elevation in the junctional GluRIIA immunoreactivity that is primarily attributable to an increase in the number of GluRIIA-positive synapses (similar to a GluRIIA^Scer\UAS.cPa Scer\GAL4^Mhc.PW mutant) and strengthened junctional signal transmission. Neuromuscular junctions (NMJs) of pAbp^k10109/+ animals exhibit unaltered postsynaptic sensitivity compared with wild-type NMJs, but significantly larger evoked responses. Thus, the junctional quantal content is significantly larger at pAbp^k10109/+ NMJs compared to wild-type and is associated with an elevated frequency of spontaneous vesicle fusion events. pAbp^k10109/+ animals exhibit enlarged larval stage neuromuscular junctions (NMJs). This larger size of NMJ is evident in a significant increase in the number of synaptic boutons, which are wild-type in shape and size.

(Sigrist et al., 2002)

The mean amplitude of miniature postsynaptic currents (mEJCs) at the neuromuscular junction is indistinguishable from wild type in heterozygotes. Evoked postsynaptic currents (eEJCs) in heterozygotes are significantly larger than in wild-type. The number of junctional boutons per neuromuscular junction is increased compared to wild type.

(Sigrist et al., 2000)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

pAbp^k10109 has abnormal cytokinesis phenotype, enhanceable by hyd[+]/hyd¹⁵

(Pertceva et al., 2010)

pAbp^k10109 has abnormal cytokinesis phenotype, enhanceable by hyd[+]/hyd^hs1

(Pertceva et al., 2010)

pAbp^k10109 has abnormal cell growth | dominant phenotype, enhanceable by Paip2^UAS.Tag:HA/Scer\GAL4^Bx-MS1096

(Roy et al., 2004)

pAbp^k10109 has visible | dominant phenotype, enhanceable by Paip2^UAS.Tag:HA/Scer\GAL4^Bx-MS1096

(Roy et al., 2004)

Enhancer of

Statement

Reference

pAbp[+]/pAbp^k10109 is an enhancer of neoplasia | adult stage | male phenotype of tut⁴

(Shan et al., 2017)

pAbp[+]/pAbp^k10109 is an enhancer of abnormal cytokinesis phenotype of hyd¹⁵

(Pertceva et al., 2010)

pAbp[+]/pAbp^k10109 is an enhancer of abnormal cytokinesis phenotype of hyd^hs1

(Pertceva et al., 2010)

Suppressor of

Statement

Reference

pAbp[+]/pAbp^k10109 is a suppressor of visible phenotype of upd1^GMR.PB

(Mukherjee et al., 2006)

pAbp^k10109 is a suppressor of abnormal neurophysiology phenotype of GluRIIA^AD9

(Sigrist et al., 2002)

Phenotype Manifest In

Enhanced by

Statement

Reference

pAbp^k10109 has wing phenotype, enhanceable by Paip2^UAS.Tag:HA/Scer\GAL4^Bx-MS1096

(Roy et al., 2004)

Suppressed by

Statement

Reference

BicD¹, pAbp[+]/pAbp^k10109 has embryo phenotype, suppressible by pAbp^+t7.8

(Vazquez-Pianzola et al., 2011)

Enhancer of

Statement

Reference

pAbp[+]/pAbp^k10109 is an enhancer of testis phenotype of tut⁴

(Shan et al., 2017)

pAbp[+]/pAbp^k10109 is an enhancer of spermatogonium phenotype of tut⁴

(Shan et al., 2017)

Suppressor of

Statement

Reference

pAbp[+]/pAbp^k10109 is a suppressor of embryo phenotype of BicD¹

(Vazquez-Pianzola et al., 2011)

pAbp[+]/pAbp^k10109 is a suppressor of eye phenotype of Fmr1^sev.PW

(Cziko et al., 2009)

pAbp[+]/pAbp^k10109 is a suppressor of eye phenotype of upd1^GMR.PB

(Mukherjee et al., 2006)

Other

Statement

Reference

hyd^hs1, pAbp[+]/pAbp^k10109 has nucleus phenotype

(Pertceva et al., 2010)

hyd^hs1, pAbp[+]/pAbp^k10109 has elongation stage spermatid phenotype

(Pertceva et al., 2010)

hyd[+]/hyd¹⁵, pAbp^k10109 has nucleus phenotype

(Pertceva et al., 2010)

hyd[+]/hyd¹⁵, pAbp^k10109 has elongation stage spermatid phenotype

(Pertceva et al., 2010)

hyd[+]/hyd^hs1, pAbp^k10109 has nucleus phenotype

(Pertceva et al., 2010)

hyd[+]/hyd^hs1, pAbp^k10109 has elongation stage spermatid phenotype

(Pertceva et al., 2010)

hyd¹⁵, pAbp[+]/pAbp^k10109 has nucleus phenotype

(Pertceva et al., 2010)

hyd¹⁵, pAbp[+]/pAbp^k10109 has elongation stage spermatid phenotype

(Pertceva et al., 2010)

Additional Comments

Genetic Interactions

Statement

Reference

The severity of the tut⁴ mutant tumorigenic phenotype is also strongly enhanced by combination with a single copy of pAbp^k10109, but if combined with just one copy of tut⁴, this genetic perturbation does not cause a significant tumor phenotype.

(Shan et al., 2017)

The BicD¹/+ mutant embryonic phenotypes are suppressed by pAbp^k10109/+.

The suppression of the BicD¹/+ embryonic phenotypes by pAbp^k10109/+ is partially reverted by one copy of pAbp^+t7.8.

(Vazquez-Pianzola et al., 2011)

pAbp^k10109/hyd¹⁵ trans-heterozygous double mutants exhibit spermatogenesis defects. The morphology of nuclei in the sperm head bundle are indistinguishable from the control but the nuclei are frequently scattered abnormally. Cytokinetic abnormalities are also increased in these double mutants.

pAbp^k10109/hyd^hs1 trans-heterozygous double mutants exhibit spermatogenesis defects. Approximately 30% of head bundles in the sperm contain both round- and needle-shaped nuclei. Abnormal nuclei scattering occurs at low frequency. Cytokinetic abnormalities are also increased in these double mutants.

(Pertceva et al., 2010)

The elimination of one copy of GluRIIA in pAbp^k10109/+, GluRIIA^AD9/+ mutants results in an almost complete suppression of enhanced junctional signal transmission and in a corresponding suppression of junctional growth, indicating that animals with genetically restricted GluRIIA expression are incapable of developing a strengthened larval stage neuromuscular junction.

(Sigrist et al., 2002)

Xenogenetic Interactions

Statement

Reference

Scer\GAL4^elav-PG159-mediated expression of Avic\GFP^{Cameleon2.0.Scer\UAS} does not affect the phenotype of pAbp^k10109/+ mutant larvae: these mutants still have larger evoked postsynaptic currents and significantly more boutons compared to wild type.

(Reiff et al., 2002)

Complementation and Rescue Data

Rescued by

pAbp^k10109 is rescued by pAbp^+t7.8

(Vazquez-Pianzola et al., 2011)

Comments

pAbp^+t7.8 rescues the germline clone phenotypes and the zygotic lethality of pAbp^k10109.

(Vazquez-Pianzola et al., 2011)

Images (0)

Mutant

Wild-type

Stocks (3)

Bloomington

10970

y¹ w^67c23; P{lacW}pAbp^k10109/CyO

98092

w^*; P{FRT(w^hs)}G13 P{lacW}pAbp^k10109/SM1; M{UASp-pAbp.myc}ZH-64A/TM3, Sb¹

Kyoto

111280

y^d2 w¹¹¹⁸ P{ey-FLP.N}2 P{5xglBS-lacZ.38-1}TPN1; P{neoFRT}42D P{lacW}pAbp^k10109 /CyO y⁺

Notes on Origin

Discoverer

I. Kiss.

(BDGP Project Members, 1994-1999)

Comments

Precise excision of the P{lacW} element restores viability and reverts the morphological phenotypes of pAbp^k10109 heterozygotes close to wild type.

(Sigrist et al., 2000)

Complements: Hsf⁰³⁰⁹¹. Complements: sbb⁰⁴⁴⁴⁰. Complements: lolal^k02512. Complements: l(2)k08931^k08931. Complements: lolal^k11212. Complements: Pcl^s1859.

(BDGP Project Members, 1994-1999)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (10)

Reported As

Symbol Synonym

P(10970)

(Roy et al., 2004)

P970

(Sigrist et al., 2000)

k10109

(Mukherjee et al., 2006)

l(2)k10109

(Doane, 2000, Spradling et al., 1999)

l(2)k10109^k10109

(BDGP Project Members, 1994-1999)

pAbp^K10109

(Singh et al., 2022)

pAbp^k10109

(Shan et al., 2017, Chartier et al., 2015, Singh et al., 2011, Pertceva et al., 2010, Blagden et al., 2009)

pabp^<up>K10109</up>

(Cziko et al., 2009)

pabp^P970

(Sigrist et al., 2003, Reiff et al., 2002, Sigrist et al., 2002)

pabp^k10109

(Sofola et al., 2007)

Name Synonyms

Secondary FlyBase IDs

References (19)

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