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Variable Glutamine-Rich Repeats Modulate Transcription Factor Activity.

Rita Gemayel1, Sreenivas Chavali2, Ksenia Pougach1

  • 1Laboratory of Systems Biology, VIB, Gaston Geenslaan 1, 3001 Heverlee, Belgium; Laboratory of Genetics and Genomics, Centre of Microbial and Plant Genetics (CMPG), Department M2S, KU Leuven, Gaston Geenslaan 1, 3001 Heverlee, Belgium.

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Glutamine (Q)-rich repeats in proteins modulate gene transcription factor function. Moderate variations cause phenotypic changes, while excessive expansions lead to neurodegenerative diseases and protein aggregation.

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Area of Science:

  • Molecular Biology
  • Genetics
  • Neuroscience

Background:

  • Polyglutamine (Q)-rich repeats are implicated in neurodegenerative diseases like Huntington's disease.
  • The physiological roles of Q-rich repeats and moderate repeat variations are not well understood.

Purpose of the Study:

  • To investigate the functional role of Q-rich domains in eukaryotic transcription factors.
  • To determine the consequences of moderate repeat variations in Q-rich domains.

Main Methods:

  • Analysis of Q-rich domains in eukaryotic transcription factors.
  • Systematic variation of Q-rich repeats in the yeast transcriptional regulator Ssn6 (Cyc8).
  • Quantitative proteomic analysis to assess protein solubility and interactions.

Main Results:

  • Q-rich domains are enriched in transcription factors and modulate their function.
  • Incremental changes in Ssn6 repeat length caused systematic, repeat-length-dependent gene expression changes and phenotypic variation.
  • Ssn6 function increased with repeat number up to a threshold, beyond which aggregation occurred.
  • Proteomic analysis showed Ssn6 repeats influence solubility and interactions with Tup1.

Conclusions:

  • Q-rich repeats are dynamic functional domains that modulate the innate function of regulators.
  • Moderate variations in Q-rich repeats can alter gene expression and phenotype.
  • Expansion of Q-rich repeats carries the risk of pathogenic aggregation and neurodegeneration.