FlyBase Allele Report: Dmel\p38a[1]

General Information

Symbol

Dmel\p38a¹

Species

D. melanogaster

Name

FlyBase ID

FBal0182635

Feature type

allele

Associated gene

Dmel\p38a

Associated Insertion(s)

Carried in Construct

Also Known As

Δp38a, Mpk2¹

Key Links

Allele class

loss of function allele

amorphic allele - molecular evidence

Mutagen

Delta2-3 transposase

Nature of the Allele

Allele class

amorphic allele - molecular evidence

(Schoborg et al., 2013, Chen et al., 2010)

loss of function allele

(Craig et al., 2004)

Mutagen

Delta2-3 transposase

(Craig et al., 2004)

Progenitor genotype

P{EP}CG6178^EP3637

(Craig et al., 2004)

P{EP}EP3637-2

(Craig et al., 2004)

Caused by aberration

Df(3R)p38a-c^del

Cytology

Description

Deletion with one breakpoint in Mpk2 and the other in p38c.

(Chen et al., 2010)

P{EP}CG6178^EP3637 is precisely excised and P{EP}EP3637-2 imprecisely excised creating a complete deletion of Mpk2 but leaving flanking CG31133 and CG6178 intact.

(Craig et al., 2004)

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 ( 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 heat stress response

(Cai et al., 2011)

abnormal heat stress response | adult stage

(Gonda et al., 2012)

abnormal heat stress response | recessive

(Cully et al., 2010)

abnormal immune response | adult stage

(Shinzawa et al., 2009)

abnormal osmotic stress response

(Cai et al., 2011)

abnormal oxidative stress response

(Cai et al., 2011, Vrailas-Mortimer et al., 2011)

abnormal starvation stress response

(Cai et al., 2011)

abnormal starvation stress response | recessive

(Cully et al., 2010)

abnormal stress response | recessive

(Craig et al., 2004)

fertile

(Craig et al., 2004)

non-enhancer of variegation

(Seong et al., 2011)

non-suppressor of variegation

(Seong et al., 2011)

partially lethal - majority die | nutrition conditional

(Seisenbacher et al., 2011)

short lived

(Vrailas-Mortimer et al., 2011)

viable

(Seisenbacher et al., 2011, Cully et al., 2010, Craig et al., 2004)

Phenotype Manifest In

Detailed Description

Statement

Reference

p38a¹ homozygous mutants do not display defects in locomotor behaviour.

Loss of p38a in p38a¹ mutants does not affect normal circadian rhythms in young animals.

(Vrailas-Mortimer et al., 2014)

Maximum bouton diameter at the neuromuscular junction in mutant larvae is not significantly different from that of controls.

Mutant larvae show a mild defect in axonal transport.

The ability of injured axons to sprout after injury is normal in mutant larvae.

(Klinedinst et al., 2013)

Mutant adults are more susceptible to sustained 37[o]C heat shock than wild-type flies, becoming catatonic and unresponsive more rapidly, with nearly 100% of the animals affected after 4 hours.

(Gonda et al., 2012)

Mutant adults show reduced resistance to osmotic stress, 37[o]C heat shock, dry starvation and oxidative stress compared to wild type.

(Cai et al., 2011)

Homozygous embryos do not show significant defects in ventral furrow formation.

(Mathew et al., 2011)

Very few Mpk2¹ mutant larvae exhibit a melanotic phenotype in the posterior hindgut, either under normal food conditions or in response to salt stress. Survival rates are larvae raised on normal food are comparable to wild type, but an increase in mortality rates is seen in response to severe salt stress (O.2M NaCl).

(Seisenbacher et al., 2011)

Mpk2¹ heterozygotes do not affect w silencing in the In(1)w^m4 line.

(Seong et al., 2011)

Mpk2¹ mutants have significantly reduced lifespans compared to controls.

p38b^Δ45 mutant flies are marginally less sensitive to oxidative stress (exposure to hydrogen peroxide through continuous feeding) compared to controls.

(Vrailas-Mortimer et al., 2011)

Adult survival is normal when homozygous larvae are raised on food containing high salt.

Adult homozygotes are abnormally sensitive to hydrogen peroxide, dry starvation, and high temperatures.

Survival to adulthood is significantly reduced when homozygous larvae are raised on low-nutrient food.

(Cully et al., 2010)

Mpk2¹ homozygous adults shows increased Salmonella-induced mortality over controls.

(Shinzawa et al., 2009)

Homozygotes show no developmental abnormalities, patterning or apoptosis abnormalities in nervous system or leg, wing, or eye imaginal discs. Shows reduced resistance to dry starvation, and increased susceptibility to heat shock and oxidative stress. There is no effect on survival of high osmolarity (0.2M NaCl).

(Craig et al., 2004)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

p38a¹ has partially lethal - majority die | nutrition conditional phenotype, enhanceable by MAPk-Ak2^Δ43

(Seisenbacher et al., 2011)

Suppressed by

Statement

Reference

p38a¹, p38b^Δ25 has short lived phenotype, suppressible by p38b^UAS.cAa/Scer\GAL4^Mef2.PR

(Vrailas-Mortimer et al., 2011)

p38a¹, p38b^Δ25 has abnormal oxidative stress response phenotype, suppressible by p38b^UAS.cAa/Scer\GAL4^Mef2.PR

(Vrailas-Mortimer et al., 2011)

p38a¹, p38b^Δ25 has partially lethal - majority die phenotype, suppressible by p38b^UAS.cAa/Scer\GAL4^Mef2.PR

(Vrailas-Mortimer et al., 2011)

p38a¹, p38b^Δ25 has partially lethal - majority die phenotype, suppressible by Sod2^UAS.cMa/Scer\GAL4^Mef2.PR

(Vrailas-Mortimer et al., 2011)

p38a¹, p38b^Δ25 has abnormal locomotor behavior | adult stage phenotype, suppressible by p38b^UAS.cAa/Scer\GAL4^Mef2.PR

(Vrailas-Mortimer et al., 2011)

NOT suppressed by

Statement

Reference

p38a¹, p38b^Δ25 has abnormal locomotor behavior | adult stage phenotype, non-suppressible by Scer\GAL4^elav-C155/p38b^UAS.cAa

(Vrailas-Mortimer et al., 2011)

p38a¹, p38b^Δ25 has short lived phenotype, non-suppressible by Scer\GAL4^elav-C155/p38b^UAS.cAa

(Vrailas-Mortimer et al., 2011)

p38a¹, p38b^Δ25 has partially lethal - majority die phenotype, non-suppressible by p38b^ala.UAS/Scer\GAL4^Mef2.PR

(Vrailas-Mortimer et al., 2011)

p38a¹, p38b^Δ25 has partially lethal - majority die phenotype, non-suppressible by Sod1^UAS.cAa/Scer\GAL4^Mef2.PR

(Vrailas-Mortimer et al., 2011)

p38a¹, p38b^Δ25 has partially lethal - majority die phenotype, non-suppressible by Cat^UAS.cAa/Scer\GAL4^Mef2.PR

(Vrailas-Mortimer et al., 2011)

Suppressor of

Statement

Reference

p38a¹ is a suppressor of abnormal neuroanatomy | larval stage phenotype of hiw^ND8

(Klinedinst et al., 2013)

Other

Statement

Reference

p38a¹, p38b^Δ25 has abnormal circadian rhythm phenotype

(Vrailas-Mortimer et al., 2014)

p38a¹, p38b^Δ25 has abnormal neuroanatomy | larval stage phenotype

(Klinedinst et al., 2013)

MAPk-Ak2^Δ43, p38a¹ has melanotic mass phenotype | larval stage | nutrition conditional phenotype

(Seisenbacher et al., 2011)

p38a¹, p38b^Δ25/p38b[+] has abnormal stress response phenotype

(Vrailas-Mortimer et al., 2011)

p38a¹, p38b^Δ25 has abnormal stress response phenotype

(Vrailas-Mortimer et al., 2011)

p38a¹, p38b^Δ25 has abnormal heat stress response phenotype

(Vrailas-Mortimer et al., 2011)

p38a¹, p38b^Δ25 has abnormal flight phenotype

(Vrailas-Mortimer et al., 2011)

p38a¹, p38b^Δ25 has abnormal starvation stress response phenotype

(Vrailas-Mortimer et al., 2011)

p38a¹, p38b^Δ25 has abnormal oxidative stress response phenotype

(Vrailas-Mortimer et al., 2011)

p38a¹, p38b^Δ25 has lethal | pupal stage | conditional phenotype

(Vrailas-Mortimer et al., 2011)

p38a¹, p38b^Δ45 has lethal phenotype

(Vrailas-Mortimer et al., 2011)

p38a¹, p38b^Δ25/p38b[+] has abnormal size | pupal stage | conditional phenotype

(Vrailas-Mortimer et al., 2011)

p38a¹, p38b^Δ25 has abnormal locomotor behavior | adult stage phenotype

(Vrailas-Mortimer et al., 2011)

p38a¹, p38b^Δ25 has partially lethal - majority die phenotype

(Vrailas-Mortimer et al., 2011)

p38a¹, p38b^Δ25 has short lived phenotype

(Vrailas-Mortimer et al., 2011)

p38a¹, p38b^d27 has lethal | third instar larval stage phenotype

(Cully et al., 2010)

p38a¹, p38b^d27 has decreased cell size | somatic clone | cell autonomous phenotype

(Cully et al., 2010)

p38a¹, p38b^ex9 has lethal phenotype

(Shinzawa et al., 2009)

Phenotype Manifest In

Suppressor of

Statement

Reference

p38a¹ is a suppressor of NMJ bouton | larval stage phenotype of hiw^ND8

(Klinedinst et al., 2013)

p38a¹ is a suppressor of neuromuscular junction | larval stage phenotype of hiw^ND8

(Klinedinst et al., 2013)

NOT Suppressor of

Statement

Reference

p38a¹, Scer\GAL4^BG380, p38b^DN.UAS is a non-suppressor of neuromuscular junction phenotype of hiw^ND8

(Collins et al., 2006)

p38a¹, Scer\GAL4^BG380, p38b^DN.UAS is a non-suppressor of bouton phenotype of hiw^ND8

(Collins et al., 2006)

Other

Statement

Reference

p38a¹, p38b^Δ25 has NMJ bouton | larval stage phenotype

(Klinedinst et al., 2013)

MAPk-Ak2^Δ43, p38a¹ has embryonic/larval hindgut | posterior | larval stage | nutrition conditional phenotype

(Seisenbacher et al., 2011)

p38a¹, p38b^Δ25/p38b[+] has pupa | conditional phenotype

(Vrailas-Mortimer et al., 2011)

Additional Comments

Genetic Interactions

Statement

Reference

p38b^Δ25/p38a¹ heterozygous mutants do not display defects in locomotor behaviour.

A significant proportion of p38b^Δ25/p38a¹ heterozygous mutants display arrhythmic circadian behaviour.

Approximately 38% of p38b^Δ25/p38a¹ heterozygous mutants display ultradian rhythms compared with 4% of wild-type controls.

(Vrailas-Mortimer et al., 2014)

p38b^Δ25 ; Mpk2¹ larvae show an increase in maximum bouton diameter at the neuromuscular junction compared to controls.

Mpk2¹ suppresses the increase in branch and bouton number at the neuromuscular junction which is seen in hiw^ND8 larvae.

(Klinedinst et al., 2013)

MAPk-Ak2^Δ43 Mpk2¹ double mutant larvae exhibit a weak melanotic phenotype under normal food conditions. A "black dot" is seen in the posterior hindgut in approximately 6% of larvae. The number of larvae displaying black dots increases in response to salt stress. The semi-lethality seen in Mpk2¹ mutants in response to salt stress is enhanced by MAPk-Ak2^Δ43.

(Seisenbacher et al., 2011)

p38b^Δ25 Mpk2¹ double mutant adults appear normal on eclosion but have a severely reduced lifespan compared to controls.

Expression of p38b^Scer\UAS.cAa in muscles under the control of Scer\GAL4^Mef2.PR significantly rescues the reduction in lifespan seen in p38b^Δ25 Mpk2¹ double mutants. No rescue is seen when p38b^Scer\UAS.cAa is expressed in neurons under the control of Scer\GAL4^elav-C155.

p38b^Δ25 Mpk2¹ double mutant females exhibit age-dependent impairment in flight behaviour. Negative geotaxis is also prominently impaired and deteriorates more rapidly with age. Aberrant walking behaviour is seen, with 3 day old p38b^Δ25 Mpk2¹ double mutants exhibiting various distortions that include a tendency to drag the abdomen, dragging a leg, shuffling of the metathoracic legs and frequent slippage. Walking speed is reduced compared to controls and the improvement in walking ability with age seen in wild type flies does not occur.

Expression of p38b^Scer\UAS.cAa in muscles under the control of Scer\GAL4^Mef2.PR suppresses the geotaxis and walking defects seen in p38b^Δ25 Mpk2¹ double mutant females. No suppression is seen when p38b^Scer\UAS.cAa is expressed pan-neuronally under the control of Scer\GAL4^elav-C155.

No age-dependent deterioration in the function of the giant-fiber system is observed in p38b^Δ25 Mpk2¹ double mutants.

Almost all p38b^Δ25 Mpk2¹ 1-2 day old double mutant flies die within 24 hours of heat shock at 37[o]C for 5 hours, in contrast to an almost 100% survival rate in controls. When reared under conditions of dry starvation, 50% of p38b^Δ25 Mpk2¹ double mutant animals die within 15 hours, compared to 20% of controls.

p38b^Δ25 Mpk2¹ double mutant flies are significantly more sensitive to hydrogen peroxide-induced oxidative stress compared to controls. Lifespan is also reduced when adult flies are exposed to the oxidising herbicide paraquat.

Expression of p38b^Scer\UAS.cAa in muscles under the control of Scer\GAL4^Mef2.PR significantly rescues the increased sensitivity to hydrogen peroxide-induced oxidative stress seen in p38b^Δ25 Mpk2¹ double mutants.

Only 17% of p38b^Δ25 Mpk2¹ double mutant flies make it to adulthood compared to controls.

Expression of p38b^Scer\UAS.cAa in muscles under the control of Scer\GAL4^Mef2.PR completely rescues the reduced viability seen in p38b^Δ25 Mpk2¹ double mutants.

Expression of p38b^ala.Scer\UAS in muscles under the control of Scer\GAL4^Mef2.PR does not suppress the reduction in viability seen in p38b^Δ25 Mpk2¹ double mutants.

Expression of Sod2^Scer\UAS.cMa under the control of Scer\GAL4^Mef2.PR partially rescues the reduced viability seen in p38b^Δ25 Mpk2¹ double mutants.

Expression of Sod^Scer\UAS.cAa under the control of Scer\GAL4^Mef2.PR does not rescue the reduced viability seen in p38b^Δ25 Mpk2¹ double mutants.

Expression of Cat^Scer\UAS.cAa under the control of Scer\GAL4^Mef2.PR does not rescue the reduced viability seen in p38b^Δ25 Mpk2¹ double mutants.

p38b^Δ25 Mpk2¹ double mutants fail to eclose when grown under chronic hypoxic conditions. Lifespan is equally short in hypoxic and normoxic conditions.

Homozygous Mpk2¹ mutants with one copy of p38b^Δ25 have smaller pupae and adults under hypoxic conditions compared to normoxia.

(Vrailas-Mortimer et al., 2011)

p38b^d27, Mpk2¹ double mutants die 96-120 hours after egg lay.

p38b^d27 wing disc clones induced in a Mpk2¹ background contain cells that are approximately 15% smaller than heterozygous cells in the same tissue. In contrast, their cell cycle profiles are wild type.

(Cully et al., 2010)

p38b^ex9, Mpk2¹ animals are embryonic lethal.

(Shinzawa et al., 2009)

Shows no interaction with bsk¹ or bsk².

(Craig et al., 2004)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Partially rescued by

p38a¹ is partially rescued by p38a^hs.PH

(Craig et al., 2004)

Comments

Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

8822

w^*; P{neoFRT}82B p38a¹

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (10)

Reported As

Symbol Synonym

Dmp38a null

(Shinzawa et al., 2009)

Mpk2¹

(Gomez et al., 2012, Davis et al., 2008)

p38Ka^del

(Vrailas-Mortimer et al., 2011)

p38a KO

(Cai et al., 2011)

p38a-KO

(Ha et al., 2009)

p38a¹

(Scepanovic et al., 2021, Liaw and Chiang, 2019, Maier et al., 2019, Khan et al., 2017, Santabárbara-Ruiz et al., 2015, Gonda et al., 2012, Mathew et al., 2011, Seisenbacher et al., 2011, Seong et al., 2011, Chen et al., 2010, Cully et al., 2010, Ha et al., 2009, Shimizu et al., 2008, Craig et al., 2004)

p38a^del

(Schoborg et al., 2013)

p38a^Δ

(Klinedinst et al., 2013)

Δp38Ka

(Vrailas-Mortimer et al., 2014)

Δp38a

(Klinedinst et al., 2013, Collins et al., 2006)

Name Synonyms

Secondary FlyBase IDs

References (24)

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