Molecular genetics is the study of the location, expression, function, and structure of genes. Molecular genomics applies these concepts to whole genomes or systems by asking how gene expression changes with an individual or disease. An individual’s phenotype, or observable expression of the genotype, is a way of investigating the underlying molecular structure.
C. elegans has long been used as a model organism in the study of molecular genetics. Using modern genetic techniques, mutations and clinical variants can quickly be introduced. Researchers can easily use the map of the C. elegans genome to generate and explore hypotheses.
Introducing the ScreenChip System: a platform for molecular genetics and genomics
Visualize gene disruption to determine gene function in a multicellular organism. Quantitative phenotypic measurements reveal that mutations in the mod-5 gene, a homolog of human SLC6A4, have distinctly different pharyngeal pumping that is three times the normal rate.
The ScreenChip phenotyping platform enables you to:
- Obtain rapid, automated data acquisition and analysis from your worms
- Discover unexplored behavioral outputs for genetically modified worm populations
- Measure the effects of genetic alterations in a rapidly developing organism
Key advantages of the ScreenChip system phenotyping assays:
- Directly quantify and measure the phenotypic readout from genetic manipulation to gene structure and function (Fig. 1)
- Observe the effects on gene expression and determine behavioral responses (Fig. 2)
- Examine genetic mechanisms from many experimental angles (Fig. 3)
- Get accurate, real-time genomic data with robust sample sizes (Fig. 4)
Directly quantify and measure the phenotypic readout from genetic manipulation to gene structure and function
Fig. 1: EPG data from humanized mod-5 mutants (a RediMODEL Kit created by Knudra Transgenics), with human homolog SLC64A expressed in the pharynx, show reduction in pumping to that which is observed in control worms.
Learn more about RediMODEL Kits from Knudra Transgenics.
Observe the effects on gene expression and determine behavioral responses
Fig. 2: Irregular pharyngeal pumping in tph-1 mutants is evident in their electric signal or EPG.
Examine genetic mechanisms from many experimental angles
Fig. 3: Genetic manipulation pre and post synapse in glutamate transporter. eat-4 encodes an ortholog of the mammalian BNPI vesicular glutamate transporter. When this signaling pathway is disrupted, as in eat-4 or avr-15 mutants, there is more than just a reduction in pumping frequency (A): mutants have a longer pump duration (B) and longer duration between pumps (C).
Get accurate, real-time genomic data with robust sample sizes
Fig. 4: Reduced mean pumping frequency observed for tph-1 mutants. Low pumping rate observed in tph-1 loss-of-function mutants is directly related to a decrease in endogenous production of 5HT, which stimulates and regulates pharyngeal pumping. Data were pooled over three sampling days for a total sample size of ~100 individuals.