FlyBase Allele Report: Dmel\Pex16[1]

General Information

Symbol

Dmel\Pex16¹

Species

D. melanogaster

Name

FlyBase ID

FBal0265692

Feature type

allele

Associated gene

Dmel\Pex16

Associated Insertion(s)

Carried in Construct

Key Links

Allele class

amorphic allele - genetic evidence

Mutagen

P-element activity

Nature of the Allele

Allele class

amorphic allele - genetic evidence

(Nakayama et al., 2011)

Mutagen

P-element activity

(Nakayama et al., 2011)

Progenitor genotype

P{GSV6}Pex16^GS14106

(Nakayama et al., 2011)

Cytology

Description

Imprecise excision of the progenitor insertion, resulting in a deletion that removes most of the pex16 coding region.

(Nakayama et al., 2011)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

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 ( 1 )

Disease

Evidence

References

model of Zellweger syndrome

CEA

(Nakayama et al., 2011)

model of peroxisome biogenesis disorder 8A

CEA

(Wangler et al., 2017)

Modifiers Based on Experimental Evidence ( 0 )

Disease

Interaction

References

Comments on Models/Modifiers Based on Experimental Evidence ( 1 )

The Pex16¹ mutant does not recapitulate the infant death of Zellweger syndrome.

(Nakayama et al., 2011)

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

abnormal eye color

(Nakayama et al., 2011)

abnormal flight (with Df(3L)BSC563)

(Wangler et al., 2017)

abnormal flight | recessive

(Nakayama et al., 2011)

abnormal locomotor behavior | adult stage

(Nakayama et al., 2011)

abnormal locomotor behavior | adult stage (with Df(3L)BSC563)

(Wangler et al., 2017)

abnormal locomotor behavior | adult stage (with Df(3L)ri-XT1)

(Nakayama et al., 2011)

abnormal locomotor behavior | adult stage | nutrition conditional (with Df(3L)BSC563)

(Wangler et al., 2017)

abnormal neuroanatomy

(Nakayama et al., 2011)

abnormal neurophysiology | adult stage | progressive (with Df(3L)BSC563)

(Wangler et al., 2017)

abnormal starvation stress response | adult stage (with Df(3L)BSC563)

(Wangler et al., 2017)

bang sensitive (with Df(3L)BSC563)

(Wangler et al., 2017)

decreased body size (with Df(3L)ri-XT1)

(Nakayama et al., 2011)

male sterile

(Nakayama et al., 2011)

short lived

(Nakayama et al., 2011)

short lived (with Df(3L)BSC563)

(Wangler et al., 2017)

short lived (with Df(3L)ri-XT1)

(Nakayama et al., 2011)

short lived | nutrition conditional (with Df(3L)BSC563)

(Wangler et al., 2017)

viable

(Nakayama et al., 2011)

viable (with Df(3L)ri-XT1)

(Nakayama et al., 2011)

Phenotype Manifest In

dendrite

(Nakayama et al., 2011)

embryonic/larval salivary gland | larval stage (with Df(3L)BSC563)

(Wangler et al., 2017)

lobula plate

(Nakayama et al., 2011)

peroxisome

(Nakayama et al., 2011)

peroxisome | larval stage (with Df(3L)BSC563)

(Wangler et al., 2017)

retina | adult stage | progressive (with Df(3L)BSC563)

(Wangler et al., 2017)

testis

(Nakayama et al., 2011)

Detailed Description

Statement

Reference

Pex16¹/Df(3L)BSC563 transheterozygotes show peroxisome biogenesis defects in larval salivary glands, as indicated by the severely decreased Pex3 punctate staining.

Pex16¹/Df(3L)BSC563 transheterozygous adults show severely reduced activity and a progressive decrease in electroretinogram amplitude (observed in 4 weeks-old adults, but not in 2 days-old adults) under standard diet, as compared to controls. These mutants survive for less time and show increased activity under either complete starvation or low-sugar diet, as compared to controls.

(Wangler et al., 2017)

Homozygotes and homozygotes lacking maternal Pex16 function are viable. Adult homozygotes have an eye colour phenotype similar to that of ry mutants.

Pex16¹/Df(3L)ri-XT1 adults are smaller than normal: mean body weight is reduced by 70% in females and 85% in males compared to wild-type controls two days after eclosion.

The Malpighian tubule cells of homozygous larvae contain peroxisome-like granules, but they are greatly reduced in number compared to wild type. Adult homozygotes show accumulation of very long chain fatty acids (VLCFAs): the level of VLCFAs with a chain length greater than C24 is two-fold higher in homozygotes compared to wild type, while the level of fatty acids with chain lengths shorter than C18 is unaffected.

Homozygous and Pex16¹/Df(3L)ri-XT1 adults climb less actively than wild type, even immediately after eclosion, in a negative geotaxis assay. The mutant flies also show a more rapid decline in climbing performance with age compared to controls. Homozygous adults show reduced flying ability compared to controls at both 2 and 10 days after eclosion.

Homozygous and Pex16¹/Df(3L)ri-XT1 adults have a severely reduced lifespan compared to controls.

Homozygous adults show structural defects of the dendritic trees in the lobula plate of the optic lobe: in contrast to wild type, areas of low-density dendrites are seen in the mutants one day after eclosion. This reduction in dendrites is detectable at the pupal stage and does not worsen at 10 days after eclosion. Other parts of the brain appear normal in the mutant flies.

Homozygous males have smaller testes than normal and do not contain any mature sperm cells. Spermatogenesis is arrested at the young apolar spermatocyte stage. Peroxisomes are absent from the spermatocytes and the cyst cells, although the cyst cells are morphologically normal.

(Nakayama et al., 2011)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

Pex16¹/Df(3L)BSC563 has short lived phenotype, suppressible by Dp(3;2)CH322-115M13

(Wangler et al., 2017)

Pex16¹/Df(3L)BSC563 has abnormal flight phenotype, suppressible by Dp(3;2)CH322-115M13

(Wangler et al., 2017)

Pex16¹/Df(3L)BSC563 has abnormal locomotor behavior | adult stage phenotype, suppressible by Dp(3;2)CH322-115M13

(Wangler et al., 2017)

Pex16¹/Df(3L)BSC563 has abnormal starvation stress response | adult stage phenotype, suppressible | partially by Dp(3;2)CH322-115M13

(Wangler et al., 2017)

Pex16¹/Df(3L)BSC563 has short lived | nutrition conditional phenotype, suppressible | partially by Dp(3;2)CH322-115M13

(Wangler et al., 2017)

Pex16¹/Df(3L)BSC563 has abnormal locomotor behavior | adult stage | nutrition conditional phenotype, suppressible by Dp(3;2)CH322-115M13

(Wangler et al., 2017)

Phenotype Manifest In

Suppressed by

Statement

Reference

Pex16¹/Df(3L)BSC376 has embryonic/larval salivary gland | larval stage phenotype, suppressible by Dp(3;2)CH322-115M13

(Wangler et al., 2017)

Pex16¹/Df(3L)BSC376 has peroxisome | larval stage phenotype, suppressible by Dp(3;2)CH322-115M13

(Wangler et al., 2017)

Additional Comments

Genetic Interactions

Statement

Reference

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

Pex16¹ is rescued by Pex16^UAS.cNa/Scer\GAL4^elav.PU/Scer\GAL4^Lsp2.PH

(Nakayama et al., 2011)

Pex16¹ is rescued by Pex16^UAS.cNa/Scer\GAL4^ptc-559.1

(Nakayama et al., 2011)

Partially rescued by

Pex16¹ is partially rescued by Pex16^UAS.cNa/Scer\GAL4^elav.PU

(Nakayama et al., 2011)

Pex16¹ is partially rescued by Pex16^UAS.cNa/Scer\GAL4^Lsp2.PH

(Nakayama et al., 2011)

Not rescued by

Pex16¹ is not rescued by Pex16^UAS.cNa/Scer\GAL4^NP5021

(Nakayama et al., 2011)

Pex16¹ is not rescued by Pex16^UAS.cNa/Scer\GAL4^{VP16.nanos.UTR}

(Nakayama et al., 2011)

Comments

Expression of Pex16^Scer\UAS.cNa under the simultaneous control of Scer\GAL4^elav.PU and Scer\GAL4^Lsp2.PH rescues the shortened lifespan, climbing defects and flight ability defects that are seen in Pex16¹ homozygotes. Expression under the control of either driver alone does not rescue these defects.

Expression of Pex16^Scer\UAS.cNa under the control of either Scer\GAL4^elav.PU or Scer\GAL4^Lsp2.PH rescues the defects in the dendritic trees of the lobula plate which are seen in Pex16¹ homozygotes.

Expression of Pex16^Scer\UAS.cNa under the control of Scer\GAL4^NP5021 does not rescue the shortened lifespan, climbing defects and flight ability defects that are seen in Pex16¹ homozygotes.

Expression of Pex16^Scer\UAS.cNa under the control of Scer\GAL4^ptc-559.1 (in the cyst cells of the testis) rescues the fertility of Pex16¹ males: morphologically normal spermatids and moving sperm are seen in these flies. Expression of Pex16^Scer\UAS.cNa under the control of Scer\GAL4^{nos.UTR.T:Hsim\VP16} (in the germline cells) does not rescue the sterility or defective spermatogenesis of Pex16¹ males.

(Nakayama et al., 2011)

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (2)

Reported As

Symbol Synonym

Pex16¹

pex16¹

(Wangler et al., 2017, Nakayama et al., 2011)

Name Synonyms

Secondary FlyBase IDs

References (2)

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