The loss of the tail in hominoids (humans and apes) is a significant evolutionary event, potentially linked to bipedalism. This study identifies a hominoid-specific Alu element insertion in the *TBXT* gene intron as a contributing factor. This insertion interacts with a neighboring Alu element, causing alternative splicing and resulting in a shorter *TBXT* isoform. Mouse models expressing this isoform exhibited tail loss or shortening, suggesting the isoform's sufficiency in inducing the phenotype. However, this isoform also led to neural tube defects, suggesting a potential evolutionary trade-off.
Publisher
Nature
Published On
Feb 29, 2024
Authors
Bo Xia, Weimin Zhang, Guisheng Zhao, Xinru Zhang, Jiangshan Bai, Ran Brosh, Aleksandra Wudzinska, Emily Huang, Hannah Ashe, Gwen Ellis, Maayan Pour, Yu Zhao, Camila Coelho, Yinan Zhu, Alexander Miller, Jeremy S. Dasen, Matthew T. Maurano, Sang Y. Kim, Jef D. Boeke, Itai Yanai
Tags
tail loss
hominoids
TBXT gene
alternative splicing
evolution
neural tube defects
Alu element
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