Characterization of harpy/Rca1/emi1 mutants: Patterning in the absence of cell division
Article first published online: 9 FEB 2010
Copyright © 2010 Wiley-Liss, Inc.
Volume 239, Issue 3, pages 828–843, March 2010
How to Cite
Riley, B. B., Sweet, E. M., Heck, R., Evans, A., McFarland, K. N., Warga, R. M. and Kane, D. A. (2010), Characterization of harpy/Rca1/emi1 mutants: Patterning in the absence of cell division. Dev. Dyn., 239: 828–843. doi: 10.1002/dvdy.22227
- Issue published online: 11 FEB 2010
- Article first published online: 9 FEB 2010
- Manuscript Accepted: 3 DEC 2009
- National Institutes of Health. Grant Number: NIDCD-DC003806
- primary neurons;
- muscle pioneers;
- neural crest;
- otic placode;
- DNA replication
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. Developmental Dynamics 239:828–843, 2010. © 2010 Wiley-Liss, Inc.