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Full-Text Articles in Life Sciences
Tumor Formation In Response To Loss Of Chromatin Remodeler Chd5 In Zebrafish, Taylor R. Sabato, Erin L. Sorlien, Dr. Joseph P. Ogas
Tumor Formation In Response To Loss Of Chromatin Remodeler Chd5 In Zebrafish, Taylor R. Sabato, Erin L. Sorlien, Dr. Joseph P. Ogas
The Summer Undergraduate Research Fellowship (SURF) Symposium
Chromodomain helicase DNA binding protein 5 (CHD5) has been identified as a tumor suppressor in humans. Deletion or mutation of CHD5 has been observed in numerous cancers, including neuroblastoma and melanoma. We hypothesize that chd5 is also a tumor suppressor in zebrafish, a powerful model system to study tumorigenesis. Many genes involved in tumorigenesis are conserved in zebrafish, and they develop fully penetrant tumor phenotypes. We have created chd5 knock-out zebrafish using CRISPR/Cas9 and are monitoring them for tumor development. In addition to the chd5 knock-outs, we are undertaking a double-mutant approach by coupling loss …
Loss Of Myod Promotes Fate Transdifferentiation Of Myoblasts Into Brown Adipocytes, Chao Wang, Weiyi Liu, Yaohui Nie, Mulan Qaher, Hannah Elizabeth Horton, Feng Yue, Atsushi Asakura, Shihuan Kuang
Loss Of Myod Promotes Fate Transdifferentiation Of Myoblasts Into Brown Adipocytes, Chao Wang, Weiyi Liu, Yaohui Nie, Mulan Qaher, Hannah Elizabeth Horton, Feng Yue, Atsushi Asakura, Shihuan Kuang
Department of Animal Sciences Faculty Publications
Brown adipose tissue (BAT) represents a promising agent to ameliorate obesity and other metabolic disorders. How- ever, the abundance of BAT decreases with age and BAT paucity is a common feature of obese subjects. As brown adipocytes and myoblasts share a common Myf5 lineage origin, elucidating the molecular mechanisms underlying the fate choices of brown adipocytes versus myoblasts may lead to novel approaches to expand BAT mass. Here we identify MyoD as a key negative regulator of brown adipocyte development. CRISPR/CAS9-mediated deletion of MyoD in C2C12 myoblasts facilitates their adipogenic transdifferentiation. MyoD knockout downregulates miR- 133 and upregulates the miR-133 …