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A human-specific insertion promotes cell proliferation and migration by enhancing TBC1D8B expression.

Hui Zhao1, Lin-Lin Liu2,3, Jian Sun4,5

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A human-specific DNA insertion, Insert-446, upregulates TBC1D8B gene expression, promoting cell proliferation and migration. This ancient genetic element, found in Neanderthals, impacts human evolution and disease.

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cell proliferation and migrationenhancergene expressionhuman-specific insertion

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Area of Science:

  • Genomics
  • Evolutionary Biology
  • Molecular Biology

Background:

  • Human-specific genomic insertions contribute to unique human traits and diseases.
  • The TBC1D8B gene, located on the X chromosome, plays a role in cellular functions.

Purpose of the Study:

  • To investigate the origin and function of a human-specific insertion (Insert-446) in the TBC1D8B gene.
  • To understand the role of Insert-446 in regulating TBC1D8B expression and its impact on cell behavior and tumorigenesis.

Main Methods:

  • Tracing the evolutionary origin of Insert-446 using ancient and comparative genomics.
  • Assessing Insert-446's enhancer activity by measuring TBC1D8B gene expression.
  • Investigating the functional consequences of TBC1D8B overexpression and knockdown in vitro and in vivo.
  • Analyzing the effect of Insert-446 knockout on cell proliferation and migration.

Main Results:

  • Insert-446, originating from the EBF1 gene, is present in Neanderthal and Denisovan genomes and fixed in humans post-divergence from chimpanzees.
  • Insert-446 functions as an enhancer, significantly increasing human TBC1D8B expression compared to macaques.
  • TBC1D8B overexpression promotes cell proliferation and migration via a catalytic mechanism.
  • Knockdown of TBC1D8B inhibits tumorigenesis, and knockout of Insert-446 prevents cell proliferation and migration.

Conclusions:

  • Human-specific Insert-446 upregulates TBC1D8B, driving cell proliferation and migration.
  • This insertion provides insights into the evolutionary impact of genetic elements on human phenotypes and disease susceptibility.