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

A deletion; the coordinates are based on Figure 5A of FBrf0056126 and differ by 2 bp from the coordinates of accession GB:L07943

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

Nucleotides 4224 to 4498 have been deleted. This produces a pum protein that lacks a RNA-binding domain.

Deletion of base pairs 4224-4498 resulting in a frame-shift and premature stop codon. Protein lacks the RNA-binding domain, required for the binding of pum to hb RNA.

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 ( 1 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
Disease-implicated variant(s)
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description

Boutons at the third instar larval neuromuscular junction of pum7/pum9 mutants are irregularly shaped, decreased in number and larger in size than controls.

pum1/pum9 ovarioles are characterised by germline-empty germaria and an egg chamber.

pum9/pum7 mutant muscle 12 1b neuromuscular junctions differ in a number of ways from wild-type. The synaptic span (the largest distance between the terminal boutons of the 1b synapse) is much smaller in these mutants, abnormally large boutons are seen in pum9/pum7 mutant 1b neuromuscular junctions, while the total number of 1b boutons is reduced, suggesting that individual boutons may fail to separate from each other during bouton division.

The average area of a type 1B bouton is increased by a factor of more than 2 in pum9/pum7 mutants. This increase in size is accompanied by a 1.8-fold decrease in the total number of type 1b boutons per neuromuscular junction. 1B neuromuscular junctions on other muscles are affected in a similar manner. No defects are observed in pum9/+ heterozygote larvae.

pum9/pum7 mutant neuromuscular junctions at muscle 6/7 in segments A2-A5 exhibit large increases in the number of eIF-4E aggregates, relative to controls. For pum9/pum7 larvae, a total of 2001 aggregates among 80 neuromuscular junctions, or 25 aggregates per neuromuscular junction are found. This represents a 5- to 12-fold increase in the number of aggregates per neuromuscular junction relative to wild-type controls. Aggregate numbers in pum9/+ heterozygote larvae do no differ significantly from wild-type.

pum9/pum7 larvae exhibit 5.4- to 12-fold more eIF-4E per muscle 6/7 neuromuscular junction than wild-type controls.

pum9/pum7 mutant larvae picked directly from liquid food exhibit large numbers of eIF-4E aggregates (15.5 aggregates per neuromuscular junction) and have eIF-4E levels that are only 36% lower than larvae induced to move from the same vial.

1s boutons increase in number by about 1.7-fold in pum9/pum7 mutants.

Quantal content, in response to evoked transmitter release, is reduced in pum9/pum7 mutants due to their elevated mEJP amplitudes. pum9/+ larvae do not display an increase in mEJP amplitudes.

The mEJP amplitude and quantal content phenotypes of pum9/pum7 mutants are not rescued to near wild-type levels by neuronal (Scer\GAL4elav-C155), muscle (Scer\GAL4Mhc.Switch.PO), or dual expression of pumScer\UAS.fl.

mEJP frequency is elevated by 1.8- to 3-fold relative to heterozygote and wild-type controls in pum9/pum7 mutants.

pumbem/pum9 transheterozygotes exhibit a significantly faster long term facilitation (LTF) at the neuromuscular junction than seen in wild-type.

External Data
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressor of

pum9/pum[+] is a suppressor of visible phenotype of Hsap\PABPN117ala.Act88F

Phenotype Manifest In
Suppressor of
Additional Comments
Genetic Interactions

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 pum9/+.

pum02003 bamΔ86/pum9 bamΔ86 double mutant ovaries have a complex phenotype that is distinct from that of either single mutant. A mixture of apparently undifferentiated cells and overtly polyploid cells is seen. In many cases, the polyploid chromosomes are thick and expanded like nurse cell chromosomes. Occasionally these pseudo-nurse cells are organised within an epithelial layer of follicle cells, like a cyst, although these cysts never contain a full complement of 16 cystocytes. These cysts contain ring canals.

Most germaria are devoid of germ cells in pum1 bamΔ86/pum9 bamΔ86 double mutant females.

Xenogenetic Interactions

pum9 suppresses the wing posture defects seen upon expression of Hsap\PABPN117ala.Act88F.

Complementation and Rescue Data
Fails to complement

Expression of pumScer\UAS.fl at 18oC in postmitotic neurons (Scer\GAL4elav-C155) rescues the synaptic morphology phenotypes found in a pum9/pum7 background. Both the average size and the number of type 1b boutons on muscle 12 are restored to wild-type.

Expression of pumScer\UAS.fl at 18oC in muscles (by 'leaky' expression of Scer\GAL4Mhc.Switch.PO in the absence of steroid) has no effect on the phenotypes found in a pum9/pum7 background.

Expression of pumScer\UAS.fl in muscles (Scer\GAL4Mhc.Switch.PO) in pum9/pum7 larvae reduces the number of eIF-4E aggregates by 7-fold, to 3.5 aggregates per neuromuscular junction. The level of eIF-4E is reduced by approximately 6.5-fold. In contrast, neural expression of pumScer\UAS.fl (Scer\GAL4elav-C155) in pum9/pum7 larvae does not greatly decrease the number of eIF-4E aggregates (although a 20% reduction is seen). Levels of eIF-4E are 88% of those in pum9/pum7 larvae.

The increase in 1s bouton number in pum9/pum7 mutants is fully rescued through expression of pumScer\UAS.fl in muscles (Scer\GAL4Mhc.Switch.PO), and is unaffected by expression in neurons (under the control of Scer\GAL4elav-C155).

The mEJP amplitude and quantal content phenotypes of pum9/pum7 mutants are not rescued to near wild-type levels by neuronal (Scer\GAL4elav-C155), muscle (Scer\GAL4Mhc.Switch.PO), or dual expression of pumScer\UAS.fl.

Expression of pumScer\UAS.fl in both neurons (Scer\GAL4elav-C155) and muscles (Scer\GAL4Mhc.Switch.PO) rescues the mEJP frequency in pum9/pum7 mutants to near the level seen in pum9/+ heterozygotes.

Expression of pumRBD.Scer\UAS at 18oC in postmitotic neurons (Scer\GAL4elav-C155) does not rescue the morphology phenotypes found in a pum9/pum7 background, in contrast to its ability to provide the early abdominal segmentation function.

Complementation tested against pumbem female sterility phenotype. pum9 was also tested against the pumbem gravitaxis, flight defects and long term facilitation (LTF) defects and found not to complement.

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Notes on Origin

Recovered on the basis of failure to complement the maternal phenotype.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
References (12)