PUBLICATION

prdm1a functions upstream of itga5 in zebrafish craniofacial development

Authors
LaMonica, K., Ding, H.L., Artinger, K.B.
ID
ZDB-PUB-150327-6
Date
2015
Source
Genesis (New York, N.Y. : 2000)   53(3-4): 270-7 (Journal)
Registered Authors
Artinger, Kristin Bruk, Ding, Hailei, LaMonica, Kristi
Keywords
and neural crest, ceratobranchials, pharyngeal arches
MeSH Terms
  • Animals
  • Animals, Genetically Modified
  • DNA-Binding Proteins/genetics
  • DNA-Binding Proteins/metabolism*
  • Embryo, Nonmammalian/cytology
  • Embryo, Nonmammalian/metabolism*
  • Face/embryology*
  • Face/physiology
  • Gene Expression Regulation, Developmental*
  • In Situ Hybridization
  • Integrin alpha5/genetics
  • Integrin alpha5/metabolism*
  • Mutation/genetics
  • Nuclear Proteins/genetics
  • Nuclear Proteins/metabolism*
  • RNA, Messenger/genetics
  • Real-Time Polymerase Chain Reaction
  • Reverse Transcriptase Polymerase Chain Reaction
  • Signal Transduction
  • Skull/embryology*
  • Skull/metabolism
  • Zebrafish/embryology*
  • Zebrafish/metabolism
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed
25810090 Full text @ Genesis
Abstract
Cranial neural crest cells are specified and migrate into the pharyngeal arches where they subsequently interact with the surrounding environment. Signaling and transcription factors, such as prdm1a regulate this interaction, but it remains unclear which specific factors are required for posterior pharyngeal arch development. Previous analysis suggests that prdm1a is required for posterior ceratobranchial cartilages in zebrafish and microarray analysis between wildtype and prdm1a mutants at 25 hours post fertilization demonstrated that integrin α5 (itga5) is differentially expressed in prdm1a mutants. Here, we further investigate the interaction between prdm1a and itga5 in zebrafish craniofacial development. In situ hybridization for itga5 demonstrates that expression of itga5 is decreased in prdm1a mutants between 18- 31 hpf and itga5 expression overlaps with prdm1a in the posterior arches, suggesting a temporal window for interaction. Double mutants for prdm1a;itga5 have an additive viscerocranium phenotype more similar to prdm1a mutants, suggesting that prdm1a acts upstream of itga5. Consistent with this, loss of posterior pharyngeal arch expression of dlx2a, ceratobranchial cartilage 2-5, and cell proliferation in prdm1a mutants can be rescued with itga5 mRNA injection. Taken together, these data suggest that prdm1a acts upstream of itga5 and are both necessary for posterior pharyngeal arch development in zebrafish. This article is protected by copyright. All rights reserved.
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