School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong
Title: Elucidating the short stature mechanisms in Werner Syndrome
Biography:
Ms. Tian Yuyao got her master degree of biochemistry from Peking University. She got her doctoral degree of biomedical sciences from the Chinese University of Hong Kong.
Werner Syndrome (WS) is an autosomal recessive genetic disorder characterized by premature aging. This disease is caused by mutations in the WRN gene. WRN gene plays a vital role in genomic stability, DNA replication and transcription. The first sign of WS is short stature. Individuals with WS have an abnormally slow growth rate, and growth stops at puberty. However, the underlying mechanisms are not well understood. Here we report a potential downstream target gene, SHOX (short-stature homeobox), was involved in the failure of bone development in Werner Syndrome. Additionally, the wrn mutant zebrafish was generated. In vivo analysis of chondrogenesis confirmed the role of wrn was crucial on bone development. And in the wrn mutant zebrafish, the expression of shox also decreased. Together, we concluded that the depletion of WRN would be one of the causes of short stature.
School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong
Title: Elucidating the short stature mechanisms in Werner Syndrome
Biography:
Ms. Tian Yuyao got her master degree of biochemistry from Peking University. She got her doctoral degree of biomedical sciences from the Chinese University of Hong Kong.
Werner Syndrome (WS) is an autosomal recessive genetic disorder characterized by premature aging. This disease is caused by mutations in the WRN gene. WRN gene plays a vital role in genomic stability, DNA replication and transcription. The first sign of WS is short stature. Individuals with WS have an abnormally slow growth rate, and growth stops at puberty. However, the underlying mechanisms are not well understood. Here we report a potential downstream target gene, SHOX (short-stature homeobox), was involved in the failure of bone development in Werner Syndrome. Additionally, the wrn mutant zebrafish was generated. In vivo analysis of chondrogenesis confirmed the role of wrn was crucial on bone development. And in the wrn mutant zebrafish, the expression of shox also decreased. Together, we concluded that the depletion of WRN would be one of the causes of short stature.