Honors College Thesis
 

Impaired epidermal homeostasis in Bcl11bR3S/R3S homozygous mutant mice

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  • BCL11B, also known as CTIP2, is a transcription factor which plays a critical role in the regulation and development of many tissues and organ systems, including the skin. A 2019 study by Goos et. al. uncovered a novel point mutation in BCL11B gene that converted the Arginine(R)-3 residue to a Serine (S) (the p.R3S mutation) in BCL11B after investigating a previously uncharacterized case of unilateral coronal craniosynostosis in a human patient. A Bcl11bR3S/R3S mouse model was subsequently developed and here we have explored the effects of the p.R3S mutation on murine epidermal development utilizing that model. Perinatal lethality exhibited in homozygous Bcl11bR3S/R3S mice restricted the study window to samples collected from the skin of post-natal day 0 (P0) mice. Results demonstrated that the Bcl11bR3S/R3S P0 skin exhibited a marked reduction in epidermal thickness coupled with significant decreases in expression of keratinocyte proliferation and early- and late-stage keratinocyte differentiation markers compared to the control mice expressing the wild type BCL11B. The striking epidermal phenotype observed in the current study warrants further elucidation of the underlying mechanisms and to what extent the p.R3S mutation disrupts murine skin homeostasis during development.
  • Key Words: BCL11B, NuRD complex, PRC2 complex, epidermis, epidermal development
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  • Pending Publication
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  • 2021-03-12 to 2023-04-13

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