daf-16;daf-28

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Genetic mutants with daf-16, daf-28 alterations

Names of genes are ordered alphabetically. For the order of interventions, please see the specific paper.

Temperature °C
20
Diet
OP50
Lifespan (days)
14.0
Lifespan change (compared to wild type)
-32.37%
Phenotype
The life span for daf-28(sa191) is significantly different from the wild type and daf-28; daf-12. The life spans for wild type and daf-12 are not significantly different. The wild-type strain is the direct parent of the daf-28(sa191) mutant.
Lifespan comparisons
Double mutant daf-16(m26);daf-28(sa191) has a lifespan of 14.0 days, while single mutant daf-16(m26) has a lifespan of 18.0 days, single mutant daf-28(sa191) has a lifespan of 23.4 days and wild type has a lifespan of 20.7 days.
Type of interaction
See methods
Enhancer, opposite lifespan effects
Citation
View abstract
Malone EA et al., 1996, Genetic analysis of the roles of daf-28 and age-1 in regulating Caenorhabditis elegans dauer formation. Genetics. 143(3):1193-205 8807293 Click here to select all mutants from this PubMed ID in the graph
Abstract
Based on environmental cues, the nervous system of Caenorhabditis elegans regulates formation of the dauer larva, an alternative larval form specialized for long-term survival under harsh conditions. Mutations that cause constitutive or defective dauer formation (Daf-c or Daf-d) have been identified and the genes ordered in a branched pathway. Most Daf-c mutations also affect recovery from the dauer stage. The semi-dominant mutation daf-28(sa191) is Daf-c but has no apparent effect on dauer recovery. We use this unique aspect of daf-28(sa191) to characterize the effects of several Daf-d and synthetic Daf-c mutations on dauer recovery. We present double mutant analysis that indicates that daf-28(sa191) acts at a novel point downstream in the genetic pathway for dauer formation. We also show that daf-28(sa191) causes a modest increase (12-13%) in life span. The phenotypes and genetic interactions of daf-28(sa191) are most similar to those of daf-2 and daf-23 mutations, which also cause a dramatic increase in life span. We present mapping and complementation data that suggest that daf-23 is the same gene as age-1, identified previously by mutations that extend life span. We find that age-1 alleles are also Daf-c at 27 degrees.

Search genes: daf-16 daf-28

Entrez ID
Symbol
GenAge
Wormbase ID

172981
daf-16
View on GenAge (daf-16)
WBGene00000912

Forkhead box protein O;hypothetical protein

Locus: CELE_R13H8.1

Wormbase description: daf-16 encodes the sole C. elegans forkhead box O (FOXO) homologue; DAF-16 functions as a transcription factor that acts in the insulin/IGF-1-mediated signaling (IIS) pathway that regulates dauer formation, longevity, fat metabolism, stress response, and innate immunity; DAF-16 regulates these various processes through isoform-specific expression, isoform-specific regulation by different AKT kinases, and differential regulation of target genes; DAF-16 can interact with the CBP-1 transcription cofactor in vitro, and interacts genetically with other genes in the insulin signaling and with daf-12, which encodes a nuclear hormone receptor; DAF-16 is activated in response to DNA damage during development and co-regulated by EGL-27, alleviates DNA-damage-induced developmental arrest by inducing DAF-16-associated element (DAE)-regulated genes; DAF-16 is broadly expressed but displays isoform-specific tissue enrichment; DAF-16 localizes to both the cytoplasm and the nucleus, with the ratio between the two an important regulator of function.

Entrez ID
Symbol
GenAge
Wormbase ID

191014
daf-28
View on GenAge (daf-28)
WBGene00000920

hypothetical protein

Locus: CELE_Y116F11B.1

Wormbase description: daf-28 encodes a beta-type insulin, mostly similar to INS-4 and INS-6 and homologous to human insulin; DAF-28 inhibits dauer formation; daf-28 mutants arrest as dauers and have downregulated signals through the DAF-2/insulin pathway; in young animals, daf-28 is expressed in ASI and ASJ neurons, which regulate dauer formation; in older animals, daf-28 expression spreads to other head neurons and to the somatic gonad; daf-28 expression is reduced by pheromone signalling, or in daf-1, daf-7, daf-11, or daf-22 mutant dauers; daf-28 mutants are dominant negative, and are suppressed by excess wild-type DAF-28, INS-4, or INS-6; normal loss-of-function daf-28 alleles are expected to have a normal phenotype because C. elegans' 38 insulin genes are likely to be redundant; daf-28 expression is increased in daf-6, osm-1, or tax-4 mutants; the transmembrane protein-tyrosine phosphatase IDA-1 is required for DAF-28 function; a ida-1 null allele enhances daf-28(sa191), with double mutants forming 50% dauers at 22.5 deg. C.

Orthologs of daf-16;daf-28 in SynergyAge

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Species	Gene

Not in SynergyAge
Species	Gene

Orthologs of daf-16 in SynergyAge

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Species	Gene

Not in SynergyAge
Species	Gene
Mus musculus	Foxo6
Mus musculus	Foxo1
Mus musculus	Foxo4
Mus musculus	Foxo3

Orthologs of daf-28 in SynergyAge

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Species	Gene