Characterization of harpy/Rca1/emi1 mutants: patterning in the absence of cell division
- Authors
- Riley, B.B., Sweet, E.M., Heck, R., Evans, A., McFarland, K.N., Warga, R.M., and Kane, D.A.
- ID
- ZDB-PUB-130514-1
- Date
- 2010
- Source
- Developmental Dynamics : an official publication of the American Association of Anatomists 239(3): 828-843 (Journal)
- Registered Authors
- Heck, Rebecca, Kane, Donald A., McFarland, Karen, Riley, Bruce, Sweet, Elly, Warga, Rachel M.
- Keywords
- zebrafish, endoreduplication, primary neurons, muscle pioneers, neural crest, otic placode, pronephros, DNA replication
- MeSH Terms
-
- Alleles
- Anaphase
- Animals
- Body Patterning*
- Bromodeoxyuridine/pharmacology
- Cell Cycle Proteins/metabolism*
- Cell Differentiation
- Cell Division
- Cell Lineage
- Gene Expression Regulation, Developmental*
- Genotype
- Mutation*
- Neurons/metabolism
- Time Factors
- Zebrafish
- Zebrafish Proteins/metabolism*
- PubMed
- 20146251 Full text @ Dev. Dyn.
We have characterized mutations in the early arrest gene, harpy (hrp), and show that they introduce premature stops in the coding region of early mitotic inhibitor1 (Rca1/emi1). In harpy mutants, cells stop dividing during early gastrulation. Lineage analysis confirms that there is little change in cell number after approximately cycle-14. Gross patterning occurs relatively normally, and many organ primordia are produced on time but with smaller numbers of cells. Despite the lack of cell division, some organ systems continue to increase in cell number, suggesting recruitment from surrounding areas. Analysis of bromodeoxyuridine incorporation shows that endoreduplication continues in many cells well past the first day of development, but cells cease endoreduplication once they begin to differentiate and express cell-type markers. Despite relatively normal gross patterning, harpy mutants show several defects in morphogenesis, cell migration and differentiation resulting directly or indirectly from the arrest of cell division.