@article{204041,
  keywords = {Animals, Mutation, Transcription Factors, Repressor Proteins, Chromatin Immunoprecipitation, DNA-Binding Proteins, Gene Expression Regulation, Developmental, Animals, Genetically Modified, Drosophila melanogaster, Protein Interaction Domains and Motifs, Drosophila Proteins, Genes, Insect, Genes, Homeobox, CCCTC-Binding Factor},
  author = {Olga Kyrchanova and Nikolay Zolotarev and Vladic Mogila and Oksana Maksimenko and Paul Schedl and Pavel Georgiev},
  title = {Architectural protein Pita cooperates with dCTCF in organization of functional boundaries in Bithorax complex},
  abstract = { Boundaries in the Bithorax complex (BX-C) of  delimit autonomous regulatory domains that drive parasegment-specific expression of homeotic genes. BX-C boundaries have two crucial functions: they must block crosstalk between adjacent regulatory domains and at the same time facilitate boundary bypass. The C2H2 zinc-finger protein Pita binds to several BX-C boundaries, including  and  To study Pita functions, we have used a boundary replacement strategy by substituting modified DNAs for the  boundary, which is located between the  and  regulatory domains. Multimerized Pita sites block  crosstalk but fail to support  regulation of  (bypass). In the case of , we used a novel sensitized background to show that the two Pita-binding sites contribute to its boundary function. Although  is from BX-C, it does not function appropriately when substituted for : it blocks crosstalk but does not support bypass. Mutation of the  Pita site disrupts blocking activity and also eliminates dCTCF binding. In contrast, mutation of the  dCTCF site does not affect Pita binding, and this mutant boundary retains partial function. },
  year = {2017},
  journal = {Development},
  volume = {144},
  pages = {2663-2672},
  month = {07/2017},
  issn = {1477-9129},
  doi = {10.1242/dev.149815},
  language = {eng},
}