A subset of SMN complex members have a specific role in tissue regeneration via ERBB pathway-mediated proliferation
- Pei, W., Xu, L., Chen, Z., Slevin, C.C., Pettie, K.P., Wincovitch, S., NISC Comparative Sequencing Program, Burgess, S.M.
- NPJ Regenerative medicine 5: 6 (Journal)
- Registered Authors
- Burgess, Shawn, Pei, Wuhong, Xu, Lisha
- Genetics, Regeneration
- MeSH Terms
- 32218991 Full text @ NPJ Regen Med
Pei, W., Xu, L., Chen, Z., Slevin, C.C., Pettie, K.P., Wincovitch, S., NISC Comparative Sequencing Program, Burgess, S.M. (2020) A subset of SMN complex members have a specific role in tissue regeneration via ERBB pathway-mediated proliferation. NPJ Regenerative medicine. 5:6.
Spinal muscular atrophy (SMA) is the most common genetic disease in children. SMA is generally caused by mutations in the gene SMN1. The survival of motor neurons (SMN) complex consists of SMN1, Gemins (2-8), and Strap/Unrip. We previously demonstrated smn1 and gemin5 inhibited tissue regeneration in zebrafish. Here we investigated each individual SMN complex member and identified gemin3 as another regeneration-essential gene. These three genes are likely pan-regenerative, since they affect the regeneration of hair cells, liver, and caudal fin. RNA-Seq analysis reveals that smn1, gemin3, and gemin5 are linked to a common set of genetic pathways, including the tp53 and ErbB pathways. Additional studies indicated all three genes facilitate regeneration by inhibiting the ErbB pathway, thereby allowing cell proliferation in the injured neuromasts. This study provides a new understanding of the SMN complex and a potential etiology for SMA and potentially other rare unidentified genetic diseases with similar symptoms.
Genes / Markers
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Engineered Foreign Genes
Errata and Notes