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Gene Interaction

Gene Interaction. “Standard” interpretation of complementation test. Hawley & Gilliland (2006) Fig. 1. Exceptions to “Non-Complementation = Allelism” Intragenic complementation (usually allele-specific) Multi-domain proteins ( e.g., rudimentary )

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Gene Interaction

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  1. Gene Interaction

  2. “Standard” interpretation of complementation test Hawley & Gilliland (2006) Fig. 1

  3. Exceptions to “Non-Complementation = Allelism” • Intragenic complementation (usually allele-specific) • Multi-domain proteins (e.g., rudimentary) • Transvection – pairing-dependent allelic complementation (stay tuned!) • Second-Site Non-Complementation (“SSNC”) • “Poisonous interactions” – products interact to form a toxic product • (usually allele-specific) • “Sequestration interactions” – product of one mutation sequesters the other to a suboptimal concentration in the cell (usually one allele-specific) • Combined haplo-insufficiency (allele non-specific)

  4. Intragenic complementation in multi-domain proteins

  5. Transvection: synapsis-dependent allele complementation E. Lewis (1954) among BX-C mutations in Drosophila Numerous other genes in Drosophila and similar phenomena observed in Neurospora, higher plants, mammals Most due to enhancer elements functioning in trans (allele-specific)

  6. Examples of body and wing yellow allele interactions Transvection (allele complementation) Fig. 2 Morris, et al. (1999) Genetics 151: 633–651.

  7. Cis-preference enhancer model (Geyer, et al., 1990) W wing enhancer B body enhancer Br bristle enhancer T tarsal claw enhancer Y2is gypsy retrotransposon insertion at the yellow gene Y1#8 780bp promoter deletion Y1 ATG start codon → CTG y2 complements y1#8 (wing & body pigmented) y2 fails to complement y1 (wing & body pale)

  8. Penetrance and expressivity contrasted Figure 6-26

  9. Variable expressivity Figure 6-27

  10. Exceptions to “Non-Complementation = Allelism” • Intragenic complementation (usually allele-specific) • Multi-domain proteins (e.g., rudimentary) • Transvection – pairing-dependent allelic complementation • Second-Site Non-Complementation (“SSNC”) • “Poisonous interactions” – products interact to form a toxic product • (usually allele-specific) • “Sequestration interactions” – product of one mutation sequesters the other to a suboptimal concentration in the cell (usually one allele-specific) • Combined haplo-insufficiency (allele non-specific)

  11. Example of a “Poisonous interaction” SSNC Non-complementation of non-allelic mutations Hawley & Gilliland (2006) Fig. 4 (after Stearns & Botstein (1988) Genetics119: 249–260)

  12. A model for synthetic lethality Figure 6-23

  13. A model for recessive epistasis Figure 6-19

  14. Recessive epistasis due to the yellow coat mutation

  15. Modifier: a second mutation that influences the phenotype of another mutation. Modifiers may make a mutant phenotype more severe (=enhancers) or less severe (=suppressors). The modifier interactions may either be recessive (requiring homozygosity at the modifier locus to modify the original phenotype) or dominant (requiring only heterozygosity at the modifier locus to modify the original phenotype).

  16. Suppression: a form of epistasis whereby the expression of one mutation (the “suppressor” mutation) normalizes the phenotype of another mutation (the “suppressed” mutation). The suppressor mutation may display no other phenotype. Intragenic suppression: “pseudo-reversion”; can be same codon or different/interacting region of gene.

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