PUBLICATION
Generation, long-term persistence, and neuronal differentiation of cells with nuclear aberrations in the adult zebrafish brain
- Authors
- Zupanc, G.K., Wellbrock, U.M., Sîrbulescu, R.F., and Rajendran, R.S.
- ID
- ZDB-PUB-090217-42
- Date
- 2009
- Source
- Neuroscience 159(4): 1338-1348 (Journal)
- Registered Authors
- Keywords
- adult neurogenesis, adult stem cells, anaphase bridge, aneuploidy, laggard, mitotic segregation defect
- MeSH Terms
-
- Adult Stem Cells/cytology
- Adult Stem Cells/physiology*
- Animals
- Brain/cytology
- Brain/physiology*
- Bromodeoxyuridine
- Cell Count
- Cell Nucleus Shape
- Cell Proliferation*
- Cell Survival/genetics
- Chromosome Aberrations*
- ELAV Proteins/metabolism
- Female
- Immunohistochemistry
- Male
- Microscopy, Confocal
- Microscopy, Fluorescence
- Neurogenesis/genetics
- Neurogenesis/physiology*
- Neurons/cytology
- Neurons/physiology
- Tyrosine 3-Monooxygenase/metabolism
- Zebrafish
- PubMed
- 19217927 Full text @ Neuroscience
Citation
Zupanc, G.K., Wellbrock, U.M., Sîrbulescu, R.F., and Rajendran, R.S. (2009) Generation, long-term persistence, and neuronal differentiation of cells with nuclear aberrations in the adult zebrafish brain. Neuroscience. 159(4):1338-1348.
Abstract
Zebrafish, like other teleosts, continuously produce new cells in numerous regions of the adult brain. Immunolabeling employing antisera against phosphorylated histone-H3 and 5-bromo-2'-deoxyuridine revealed that approximately 6-7% of such cells exhibited nuclear aberrations. These aberrations, presumably the result of mitotic segregation defects, included single and multiple laggards (both during metaphase and anaphase) and anaphase bridges. Cells with such aberrations persisted long-term and comprised, when examined 7.5 months after their generation, approximately 2.5% of the total population of adult-born cells. The drop in relative frequency of aberrations in the course of further development appears to be caused by elimination of cells with nuclear aberrations, presumably by apoptotic cell death. The cells with nuclear aberrations that persisted long-term were capable of neuronal differentiation, as demonstrated by combining anti-5-bromo-2'-deoxyuridine immunohistochemistry with immunostaining against the neuronal marker protein Hu or the enzyme tyrosine hydroxylase, a marker of catecholaminergic neurons. We hypothesize that the alterations in chromosome number and/or chromosome structure caused by nuclear aberrations do not necessarily result in loss of vital functions or in tumorigenesis. Instead, cells with such aberrations are able to undergo what appears to be normal development.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping