PUBLICATION
Cell type specific gene expression profiling reveals a role for complement component C3 in neutrophil responses to tissue damage
- Authors
- Houseright, R.A., Rosowski, E.E., Lam, P.Y., Tauzin, S.J.M., Mulvaney, O., Dewey, C.N., Huttenlocher, A.
- ID
- ZDB-PUB-201002-161
- Date
- 2020
- Source
- Scientific Reports 10: 15716 (Journal)
- Registered Authors
- Huttenlocher, Anna, Lam, Pui Ying, Rosowski, Emily E.
- Keywords
- none
- MeSH Terms
-
- Animals
- Complement C3/genetics*
- Complement C3/metabolism
- Gene Expression Profiling
- Larva/metabolism
- Neutrophils/metabolism*
- Sequence Analysis, RNA
- Signal Transduction/genetics
- Wound Healing/genetics*
- Zebrafish
- Zebrafish Proteins/genetics*
- Zebrafish Proteins/metabolism
- PubMed
- 32973200 Full text @ Sci. Rep.
Citation
Houseright, R.A., Rosowski, E.E., Lam, P.Y., Tauzin, S.J.M., Mulvaney, O., Dewey, C.N., Huttenlocher, A. (2020) Cell type specific gene expression profiling reveals a role for complement component C3 in neutrophil responses to tissue damage. Scientific Reports. 10:15716.
Abstract
Tissue damage induces rapid recruitment of leukocytes and changes in the transcriptional landscape that influence wound healing. However, the cell-type specific transcriptional changes that influence leukocyte function and tissue repair have not been well characterized. Here, we employed translating ribosome affinity purification (TRAP) and RNA sequencing, TRAP-seq, in larval zebrafish to identify genes differentially expressed in neutrophils, macrophages, and epithelial cells in response to wounding. We identified the complement pathway and c3a.1, homologous to the C3 component of human complement, as significantly increased in neutrophils in response to wounds. c3a.1-/- zebrafish larvae have impaired neutrophil directed migration to tail wounds with an initial lag in recruitment early after wounding. Moreover, c3a.1-/- zebrafish larvae have impaired recruitment to localized bacterial infections and reduced survival that is, at least in part, neutrophil mediated. Together, our findings support the power of TRAP-seq to identify cell type specific changes in gene expression that influence neutrophil behavior in response to tissue damage.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping