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Pseudoallelism: Early definition: failure of a deficiency to complement recessive alleles of more than one “gene”. Later definition: these genes must be closely linked and have similar “effects”. Take for example EB Lewis’ bithorax mutants: ubx bx pbx ubx bx pbx -It appears here that ubx, bx, and pbx are all in the same complementation group -But px and pbx complement each other… + - How could this happen? Mutations in regulatory regions, as opposed to coding regions, which we focused on for the rest of the class! Types of regulatory elements: -promoter- site of RNA polymerase binding prior to initiation of transcription -enhancer- increases utilization of a promoter by binding to an activator protein to increase gene expression -operator- can bind to either activators or repressors to either increase or decrease gene expression, respectively How can these regulatory regions function? -in cis- region on one piece of DNA controls expression of a gene on the same piece of DNA -in trans- region on one piece of DNA controls expression of a gene on another piece of DNA (transvection) How can we use this to describe what is happening in the Ubx example? Ubx gene bx pbx Ubx is a transcription factor that leads to formation of the haltere instead of wing at thorasic segment 3 (T3). Bx is an enhancer that causes expression of Ubx at the anterior part of T3. pbx is an enhancer that causes expression Ubx of the posterior part of T3. What would the following heterozygotes from the complementation test look like? ubx/ bx: anterior part of the haltere is now a wing ubx/pbx: posterior part of the haltere is now a wing bx/ pbx: wild type What does this imply about their action? The enhancers only function in cis.