ZFIN ID: ZDB-PUB-170830-2
Zebrafish sin3b mutants are viable but have size, skeletal and locomotor defects
Moravec, C.E., Yousef, H., Kinney, B.A., Salerno-Eichenholz, R., Monestime, C., Martin, B.L., Sirotkin, H.I.
Date: 2017
Source: Developmental dynamics : an official publication of the American Association of Anatomists 246(11): 946-955 (Journal)
Registered Authors: Sirotkin, Howard
Keywords: CRISPR, Sin3b, behavior, early development, zebrafish
MeSH Terms:
  • Animals
  • Body Size/genetics
  • Bone and Bones/abnormalities
  • Gait Disorders, Neurologic/genetics
  • Repressor Proteins/genetics*
  • Zebrafish
PubMed: 28850761 Full text @ Dev. Dyn.
The transcriptional co-repressor Sin3 is highly conserved from yeast to vertebrates and has multiple roles controlling cell fate, cell cycle progression, and senescence programming. Sin3 proteins recruit HDACs and other chromatin modifying factors to specific loci through interactions with transcription factors including Myc, Rest, p53 and E2F. Most vertebrates have two Sin3 family members (sin3a and sin3b), but zebrafish have a second sin3a paralogue. In mice, sin3a and sin3b are essential for embryonic development. Sin3b knockout mice show defects in growth as well as bone and blood differentiation.
To study the requirement for Sin3b during development, we disrupted zebrafish sin3b using CRISPR-Cas9, and studied the effects on early development and locomotor behavior.
Surprisingly, Sin3b is not essential in zebrafish. sin3b mutants show a decrease in fitness, small size, changes to locomotor behavior, and delayed bone development. We did not detect a role for Sin3b in cell proliferation. Our analysis of the sin3b mutant revealed a more nuanced requirement for zebrafish Sin3b than would be predicted from analysis of mutants in other species. This article is protected by copyright. All rights reserved.