Back

Retrotransposon instability dominates the acquired mutation landscape of mouse induced pluripotent stem cells

Gerdes, P.; Lim, S. M.; Ewing, A. D.; Larcombe, M. R.; Chan, D.; Sanchez-Luque, F. J.; Walkner, L.; James, C.; Knaupp, A. S.; Carreira, P. E.; Nefzger, C. M.; Lister, R.; Richardson, S. R.; Polo, J. M.; Faulkner, G. J.

2022-02-17 genomics
10.1101/2022.02.16.480772 bioRxiv
Show abstract

Induced pluripotent stem cells (iPSCs) can in principle differentiate into any cell of the body, and have revolutionized biomedical research and regenerative medicine. Unlike their human counterparts, mouse iPSCs (miPSCs) are reported to silence transposable elements (TEs) and prevent TE-mediated mutagenesis. Here we applied short-read or Oxford Nanopore Technologies (ONT) long-read genome sequencing to 38 bulk miPSC lines reprogrammed from 10 parental cell types, and 18 single-cell miPSC clones. While single nucleotide variants and structural variants restricted to miPSCs were rare, we found 83 de novo TE insertions, including examples intronic to Brca1 and Dmd. LINE-1 (L1) retrotransposons were profoundly hypomethylated in miPSCs, beyond other TEs and the genome overall, and harbored alternative protein-coding gene promoters. Treatment with the L1 inhibitor lamivudine did not hinder reprogramming and efficiently blocked endogenous retrotransposition, as detected by ONT sequencing. These experiments reveal the complete spectrum and potential significance of mutations acquired by miPSCs.

Matching journals

The top 4 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.