Abstract
TLS (also known as FUS) is an RNA-binding protein that contributes the N-terminal half of fusion oncoproteins implicated in the development of human liposarcomas and leukemias. Here we report that male mice homozygous for an induced mutation in TLS are sterile with a marked increase in the number of unpaired and mispaired chromosomal axes in premeiotic spermatocytes. Nuclear extracts from TLS(-/-) testes lack an activity capable of promoting pairing between homologous DNA sequences in vitro, and TLS(-/-) mice and embryonic fibroblasts exhibit increased sensitivity to ionizing irradiation. These results are consistent with a role for TLS in homologous DNA pairing and recombination.
Original language | English |
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Pages (from-to) | 453-462 |
Number of pages | 10 |
Journal | EMBO Journal |
Volume | 19 |
Issue number | 3 |
DOIs | |
State | Published - Feb 1 2000 |
Keywords
- Fusion oncoproteins
- Homologous recombination
- Spermatogenesis
- TLS deficiency