FlyBase Allele Report: Dmel\Nf1[P2]

Nf1^P1/Nf1^P2 male flies sleep significantly less than wild type flies, whereas females do not show consistent differences; sleep is also fragmented, as males have significantly reduced bout duration and increased bout number and females have significantly increased bout number. Both male and female Nf1^P1/Nf1^P2 flies exhibit nocturnal hyperactivity (resulting in an increase in daytime sleep and a decrease in nighttime sleep), and are arrhythmic in dark conditions. Nf1^P2/Nf1^c00617 male or female flies sleep significantly less than wild type.

(Bai and Sehgal, 2015)

Nf1^P2 males and females are significantly smaller than controls.

In training trial assays, where flies are repeatedly trained with odor avoidance assays, Nf1^P2 flies perform poorly even after 15 trials, at which point their performance is not significantly different to controls. Normalisation of Nf1^P2 performance (to take into account memory decay) required training with seven trials while the control is trained with three trials. Memory of Nf1^P2 mutants, when tested at two subsequent time points, is indistinguishable from controls.

(Buchanan and Davis, 2010)

Nf1^P2 mutants exhibit a 24-40% reduction in life span, relative to controls.Nf1^P1/Nf1^P2 transheterozygotes exhibit a life span similar to Nf1^P2 flies.

Nf1^P2 mutants exhibit a drop in physical fitness compared to controls. Nf1^P2 and Nf1^P2/Nf1^P1 flies take over 100 minutes to recover from a 20 minute 37[o]C heat stress, as shown by a locomotive index generated with a climbing assay.

Nf1^P2 mutant flies are as resistant to desiccation as controls.

Nf1^P2 mutant flies are significantly more sensitive to paraquat-induced oxidative stress, compared to controls.

Mitochondrial aconitase activities in 30-day old Nf1^P2 flies are reduced by 36% compared to controls.

The ADP-stimulated respiration rate and the derived ATP synthesis rate are reduced by approximately 50% in Nf1^P2 flies, whereas the non-ADP-stimulated respiration is unaffected.

Nf1^P1/Nf1^P2 mitochondria generate more superoxide than control mitochondria.

Exposure to Mn(III)tetrakis(4-benzoic acid) porphin and tetrakis(1,3-diethyl imidazolium-2-yl) meso-substituted manganoporphyrin (MnTDEIP) increases the survivorship of Nf1^P1/Nf1^P2 flies by approximately 50%, indicating that increased superoxide anion production is the cause of the reduced life span found in Nf1^P1/Nf1^P2 mutants. These drugs also enhance the recovery rate of locomotive performance of Nf1^P1/Nf1^P2 mutants after heat stress.

(Tong et al., 2007)

Significant 25-hour locomotor activity rhythms are detected in only 51% of Nf1^P1 flies in LD (12 hour light:12 hour dark) conditions. Flies that do show significant rhythms do not show a consistent activity peak or the anticipatory behaviour that normally accompanies the light:dark transitions.

(Williams et al., 2001)

Only 10.53% of mutant flies show weak rhythmicity in locomotor activity when kept under constant darkness conditions. Average locomotor activity is normal under these conditions. 6.67% of Nf1^P1/Df(3R)Espl3 flies show rhythmic locomotor activity under constant darkness conditions.

(Williams et al., 2001)

Flies show a significant decrease in olfactory learning performance compared to controls. Olfactory avoidance and electric-shock reactivity are similar in mutant and control flies. Mutants have a smaller body size than wild-type flies. Nf1^P2 flies show a short-term memory defect (3 and 8 hour retention).

(Guo et al., 2000)

Modulation of voltage gated K⁺ currents induced by the neuropeptide pituitary adenylyl cyclase-activating polypeptide (PACAP38) is eliminated. Application of cAMP analogs or forskolin is sufficient to restore PACAP38 enhancement of K⁺ currents.

(Guo et al., 1997)

Homozygotes are 20-25% smaller than wild type during postembryonic stages. Clones in the wings demonstrates the reduced size of wing epidermal cells reflects a cell-autonomous defect, clones in the eye show a reduced number of ommatidia of normal size and structure. Heterozygous loss of Sos or Ras85D has no effect on size of Nf1 mutant pupae, nor does expression of an activated phl mutation. In homozygotes 25% ommatidia have one or more extra photoreceptor cells. Homozygotes exhibit reduced escape response due to defects at the larval neuromuscular junction.

(The et al., 1997)

Eliminates the activation of the rut-encoded adenylyl cyclase eliminating the pituitary-adenylyl-cyclase-activating polypeptide (PACAP38) response. The defect can be fully restored by supplying drugs that stimulate the cAMP pathway prior to perfusion of PACAP38. Associative learning is defective.

(Zhong, 1997)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

Nf1^P2 has abnormal locomotor rhythm | heat sensitive phenotype, enhanceable by Mmus\Prkaca^hs.PJ

(Tong et al., 2007)

Nf1^P2 has abnormal oxidative stress response | heat sensitive phenotype, enhanceable by Mmus\Prkaca^hs.PJ

(Tong et al., 2007)

NOT Enhanced by

Statement

Reference

Nf1^P2/Nf1^P1 has abnormal sleep phenotype, non-enhanceable by SIFa³/SIFa²

(Bai et al., 2018)

Nf1^P2/Nf1^P1 has abnormal sleep phenotype, non-enhanceable by SIFa¹/SIFa[+]

(Bai et al., 2018)

Nf1^P2/Nf1^P1 has abnormal sleep phenotype, non-enhanceable by SIFa[+]/SIFa²

(Bai et al., 2018)

Nf1^P2/Nf1^P1 has abnormal sleep phenotype, non-enhanceable by SIFa³/SIFa[+]

(Bai et al., 2018)

Suppressed by

Statement

Reference

Nf1^P2/Nf1^E2 has decreased sleep | larval stage phenotype, suppressible | partially by Alk⁹/Alk[+]

(Durkin et al., 2023)

Nf1^P2 has short lived phenotype, suppressible by Mmus\Prkaca^hs.PJ

(Tong et al., 2007)

Nf1^P2 has abnormal heat stress response phenotype, suppressible by Mmus\Prkaca^hs.PJ

(Tong et al., 2007)

Nf1^P2 has abnormal locomotor rhythm phenotype, suppressible by Ras85D^e1B

(Williams et al., 2001)

Nf1^P2 has abnormal locomotor rhythm phenotype, suppressible by Sos^e2H

(Williams et al., 2001)

Nf1^P2 has abnormal locomotor rhythm phenotype, suppressible by rl^x162

(Williams et al., 2001)

Nf1^P2 has abnormal learning phenotype, suppressible by Mmus\Prkaca^hs.PJ

(Guo et al., 2000)

Nf1^P2 has abnormal memory phenotype, suppressible by Mmus\Prkaca^hs.PJ

(Guo et al., 2000)

NOT suppressed by

Statement

Reference

Nf1^P2/Nf1^P1 has abnormal circadian rhythm | adult stage phenotype, non-suppressible by Pdfr[+]/Pdfr³³⁶⁹

(Bai et al., 2018)

Nf1^P2/Nf1^P1 has abnormal circadian rhythm | adult stage phenotype, non-suppressible by Pdfr[+]/Pdfr⁵³⁰⁴

(Bai et al., 2018)

Nf1^P2/Nf1^P1 has abnormal circadian rhythm | adult stage phenotype, non-suppressible by Pdfr³³⁶⁹/Pdfr³³⁶⁹

(Bai et al., 2018)

Nf1^P2/Nf1^P1 has abnormal circadian rhythm | adult stage phenotype, non-suppressible by Pdfr⁵³⁰⁴/Pdfr⁵³⁰⁴

(Bai et al., 2018)

Nf1^P2/Nf1^P1 has abnormal sleep phenotype, non-suppressible by SIFa¹/SIFa[+]

(Bai et al., 2018)

Nf1^P2/Nf1^P1 has abnormal sleep phenotype, non-suppressible by SIFa[+]/SIFa²

(Bai et al., 2018)

Nf1^P2/Nf1^P1 has abnormal sleep phenotype, non-suppressible by SIFa³/SIFa[+]

(Bai et al., 2018)

Nf1^P2/Nf1^P1 has abnormal sleep phenotype, non-suppressible by SIFa³/SIFa²

(Bai et al., 2018)

Nf1^P2/Nf1^P1 has abnormal locomotor rhythm phenotype, non-suppressible by Alk^ts/Alk¹

(Bai and Sehgal, 2015)

Nf1^P2 has abnormal locomotor rhythm phenotype, non-suppressible by dnc^ML

(Williams et al., 2001)

Nf1^P2 has abnormal locomotor rhythm phenotype, non-suppressible by Mmus\Prkaca^hs.PJ

(Williams et al., 2001, Williams et al., 2001)

Nf1^P2 has abnormal locomotor rhythm phenotype, non-suppressible by dnc¹

(Williams et al., 2001)

Nf1^P2 has abnormal locomotor rhythm phenotype, non-suppressible by RasGAP1^A13P

(Williams et al., 2001)

Enhancer of

Statement

Reference

Nf1^P2/Nf1^P1 is an enhancer of abnormal sleep phenotype of SIFa³/SIFa²

(Bai et al., 2018)

Suppressor of

Statement

Reference

Nf1^P2/Nf1^P1 is a suppressor of abnormal sleep phenotype of Alk^GD42, Scer\GAL4^nSyb.PS

(Bai and Sehgal, 2015)

Other

Statement

Reference

Alk^ts/Alk¹, Nf1^P2/Nf1^P1 has abnormal sleep phenotype

(Bai and Sehgal, 2015)

Phenotype Manifest In

Enhanced by

Statement

Reference

Nf1^P2 has CNS surface glial cell phenotype, enhanceable by poe¹

(Yager et al., 2001)

Nf1^P2 has CNS surface glial cell phenotype, enhanceable by eag¹

(Yager et al., 2001)

Nf1^P2 has CNS surface glial cell phenotype, enhanceable by ine¹

(Yager et al., 2001)

Enhancer of

Statement

Reference

Nf1^P2 is an enhancer of CNS surface glial cell phenotype of poe¹

(Yager et al., 2001)

Nf1^P2 is an enhancer of CNS surface glial cell phenotype of ine¹

(Yager et al., 2001)

Additional Comments

Genetic Interactions

Statement

Reference

Nf1^P1 heterozygosity suppresses the shorter circadian period of Pdfr⁵³⁰⁴ and Pdfr³³⁶⁹ hemizygotes and partially suppresses the circadian arrhythmicity of Pdfr³³⁶⁹ hemizygotes, but not of Pdfr⁵³⁰⁴ hemizygotes.

(Bai et al., 2018)

Nf1^P1/Nf1^P2 mutations suppress (to different degrees) the long sleep phenotype seen in Alk^ts/Alk¹ males and females at different temperatures (18, 25 or 29[o]C). In male flies, Alk^ts/Alk¹;Nf1^P1/Nf1^P2 double mutants even sleep significantly less than wild type flies.

Alk^ts/Alk¹ does not suppress arrhythmicity (in dark conditions) in Nf1^P1/Nf1^P2 flies.

(Bai and Sehgal, 2015)

rut¹; Nf1^P2 mutants do not exhibit shorter life spans compared to rut¹ single mutants.

The lifespan of dnc¹; Nf1^P2 flies is as wild-type, indicating that the reduced life span found in Nf1^P2 mutants is the product of reduced cAMP levels. These flies also show suppression of the reduced tolerance to heat stress seen in Nf1^P2.

rut¹; Nf1^P2 flies exhibit a delay in recovery time from a 20 minute 37[o]C heat stress, as shown by a locomotive index generated with a climbing assay.

rut¹; Nf1^P2 mutant flies are significantly more sensitive to paraquat-induced oxidative stress, compared to controls.

Mitochondrial aconitase activities in 30-day old rut¹; Nf1^P2 flies are reduced by 76% compared to controls (and 36% in Nf1^P2).

The ADP-stimulated respiration rate and the derived ATP synthesis rate are reduced by approximately 50% in rut¹; Nf1^P2 flies, whereas the non-ADP-stimulated respiration is unaffected.

Superoxide levels are increased in rut¹; Nf1^P2 flies compared to controls.

(Tong et al., 2007)

The addition of ine¹ or poe¹ enhances the Nf1^P2 perineurial glial thickness phenotype. The addition of eag¹ only moderately enhances the ine¹ perineurial glial thickness phenotype.

(Yager et al., 2001)

The learning scores of rut¹; Nf1^P2 double mutant flies are similar to that of either single mutant.

(Guo et al., 2000)

Xenogenetic Interactions

Statement

Reference

The presence of the heat shock-inducible and constitutively active Mmus\Pkaca^hs.PJ suppresses the reduction in life span and reduced tolerance to heat stress seen in Nf1^P2 mutants.

Expression of Mmus\Pkaca^hs.PJ in a Nf1^P2 mutant background greatly increases the resistance to paraquat-induced oxidative stress.

Expression of constitutively active Mmus\Pkaca^hs.PJ increases mitochondrial aconitase activity by over 90%, even in the absence of Nf1 (in a Nf1^P2 mutant background).

Addition of Mmus\Pkaca^hs.PJ restores the ADP-stimulated respiration rate and the derived ATP synthesis rate in Nf1^P2 mutants to wild-type levels.

(Tong et al., 2007)

small body | pupal stage, suppressible { Hsap\NF1[Scer\UAS.cHa], Scer\GAL4[e22c] }

small body | pupal stage, suppressible { Hsap\NF1[L847P.Scer\UAS], Scer\GAL4[e22c] }

small body | pupal stage, suppressible { Hsap\NF1[R1276P.Scer\UAS], Scer\GAL4[e22c] }

small body | pupal stage, suppressible { Hsap\NF1[R1391S.Scer\UAS], Scer\GAL4[e22c] }

small body | pupal stage, suppressible { Hsap\NF1[K1423E.Scer\UAS], Scer\GAL4[e22c] }

small body | pupal stage, non-suppressible { Hsap\NF1[GRD1.Scer\UAS], Scer\GAL4[e22c] }

small body | pupal stage, non-suppressible { Hsap\NF1[GRD2.Scer\UAS], Scer\GAL4[e22c] }

small body | pupal stage, non-suppressible { Hsap\NF1[Nterm.Scer\UAS], Scer\GAL4[e22c] }

small body | pupal stage, suppressible { Hsap\NF1[ΔGRD2.Scer\UAS], Scer\GAL4[e22c] }

small body | pupal stage, suppressible { Hsap\NF1[Cterm.Scer\UAS], Scer\GAL4[e22c] }

(Hannan et al., 2006)

The short-term memory defect of Nf1^P2 flies is completely rescued by heat shock induced expression of Mmus\Pkaca^hs.PJ. Mmus\Pkaca^hs.PJ partially rescues the learning defect of Nf1^P2 when the flies are raised at room temperature, and completely rescues Nf1^P2 when it is expressed using heat shock (37^oC, 30 minutes).

(Guo et al., 2000)

Complementation and Rescue Data

Fails to complement

Nf1^E3

(Walker et al., 2006)

Nf1^E4

(Walker et al., 2006)

Nf1^E2

(Walker et al., 2006)

Nf1^E1

(Walker et al., 2006)

Rescued by

Nf1^P2/Nf1^P1 is rescued by Nf1^UAS.cdNa/Scer\GAL4^ChAT.7.4

(Bai et al., 2018)

Nf1^P2/Nf1^P1 is rescued by Scer\GAL4^nSyb.PS/Nf1^UAS.cdNa

(Bai et al., 2018)

Nf1^P2/Nf1^P1 is rescued by Scer\GAL4^nSyb.PS/Nf1^UAS.cdNa

(Bai and Sehgal, 2015)

Nf1^P2 is rescued by Nf1^hs.PT

(Tong et al., 2007)

Nf1^P2 is rescued by Nf1^hs.PT

(Yager et al., 2001)

Nf1^P2 is rescued by Nf1^hs.PT

(Guo et al., 1997)

Nf1^P2 is rescued by Nf1^hs.PT

(The et al., 1997)

Partially rescued by

Nf1^P2/Nf1^P1 is partially rescued by Scer\GAL4^c453/Nf1^UAS.cdNa

(Bai et al., 2018)

Nf1^P2/Nf1^P1 is partially rescued by Scer\GAL4^c309/Nf1^UAS.cdNa

(Bai et al., 2018)

Nf1^P2/Nf1^P1 is partially rescued by Scer\GAL4^NP2024/Nf1^UAS.cdNa

(Bai et al., 2018)

Nf1^P2/Nf1^P1 is partially rescued by Scer\GAL4^53b/Nf1^UAS.cdNa

(Bai et al., 2018)

Nf1^P2/Nf1^P1 is partially rescued by Scer\GAL4^MJ63/Nf1^UAS.cdNa

(Bai et al., 2018)

Nf1^P2/Nf1^P1 is partially rescued by Scer\GAL4^Kurs58/Nf1^UAS.cdNa

(Bai et al., 2018)

Nf1^P2 is partially rescued by Nf1^hs.PT

(Williams et al., 2001)

Nf1^P2 is partially rescued by Nf1^hs.PT

(Guo et al., 2000)

Not rescued by

Nf1^P2/Nf1^P1 is not rescued by Nf1^UAS.cdNa/Scer\GAL4^Ddc.PL

(Bai et al., 2018)

Nf1^P2/Nf1^P1 is not rescued by Scer\GAL4^Tdc2.PC/Nf1^UAS.cdNa

(Bai et al., 2018)

Nf1^P2/Nf1^P1 is not rescued by Nf1^UAS.cdNa/Scer\GAL4¹⁴⁷¹

(Bai et al., 2018)

Nf1^P2/Nf1^P1 is not rescued by Scer\GAL4^Tab2-201Y/Nf1^UAS.cdNa

(Bai et al., 2018)

Nf1^P2/Nf1^P1 is not rescued by Nf1^UAS.cdNa/Scer\GAL4^c739

(Bai et al., 2018)

Nf1^P2/Nf1^P1 is not rescued by Scer\GAL4^dimm-929/Nf1^UAS.cdNa

(Bai et al., 2018)

Nf1^P2/Nf1^P1 is not rescued by Scer\GAL4^Clk.1.5/Nf1^UAS.cdNa

(Bai et al., 2018)

Nf1^P2/Nf1^P1 is not rescued by Scer\GAL4^0911-G4/Nf1^UAS.cdNa

(Bai et al., 2018)

Nf1^P2/Nf1^P1 is not rescued by Scer\GAL4^121Y/Nf1^UAS.cdNa

(Bai et al., 2018)

Nf1^P2/Nf1^P1 is not rescued by Nf1^UAS.cdNa/Scer\GAL4^P2.4.Pdf

(Bai et al., 2018)

Comments

Expression of Nf1^{Scer\UAS.cdNa} driven by Scer\GAL4^nSyb.PS rescues the decreases in total sleep seen in Nf1^P1/Nf1^P2 male and female flies, even significantly increasing total sleep beyond wild type amounts.

(Bai and Sehgal, 2015)

The paraquat sensitivity of Nf1^P2 mutant flies is eliminated in Nf1^hs.PT/+; Nf1^P2 mutants.

Addition of Nf1^hs.PT restores the ADP-stimulated respiration rate and the derived ATP synthesis rate in Nf1^P2 mutants to wild-type levels.

Mitochondrial aconitase activity is restored by expression of Nf1^hs.PT in a Nf1^P2 mutant background.

Elevated superoxide levels in Nf1^P2 mutant flies are reduced to wild-type levels by the introduction of Nf1^hs.PT.

(Tong et al., 2007)

Phenotype is rescued by heat induced expression of Nf1^hs.PT.

(Guo et al., 1997)

The growth defect can be rescued by heat induced expression of Nf1^hs.PT.

(The et al., 1997)

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Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (3)

Reported As

Symbol Synonym

NF1^P2

(Tsai et al., 2012, Walker et al., 2006, Yager et al., 2001, Guo et al., 2000)

Nf1^P2

(Durkin et al., 2023, Moscato et al., 2020, Bai et al., 2018, Bai and Sehgal, 2015, Tong et al., 2007, Hannan et al., 2006)

nf1^P2

(Buchanan and Davis, 2010)

Name Synonyms

Secondary FlyBase IDs

References (18)

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