Samantha Shaltz

Journal article PLoS Genet · January 2026 Transposable elements (TEs) are key agents of genome evolution across all domains of life. These mobile genetic elements can cause mutations through transposition or by promoting structural rearrangements. Stress conditions can amplify TE mobility, either ... Full text Link to item Cite

DNA mutagenesis driven by transcription factor competition with mismatch repair.

Journal article Cell · October 2, 2025 Despite the remarkable fidelity of eukaryotic DNA replication, nucleotide misincorporation errors occur in every replication cycle, generating mutations that drive genetic diseases and genome evolution. Here, we show that transcription factor (TF) proteins ... Full text Link to item Cite

Temperature and genetic background drive mobilization of diverse transposable elements in a critical human fungal pathogen.

Journal article bioRxiv · May 23, 2025 Transposable elements (TEs) are key agents of genome evolution across all domains of life. These mobile genetic elements can cause mutations through transposition or by promoting structural rearrangements. Stress conditions can amplify TE activity, either ... Full text Link to item Cite

Deletions initiated by the vaccinia virus TopIB protein in yeast.

Journal article DNA repair · May 2024 The type IB topoisomerase of budding yeast (yTop1) generates small deletions in tandem repeats through a sequential cleavage mechanism and larger deletions with random endpoints through the nonhomologous end-joining (NHEJ) pathway. Vaccinia virus Top1 (vTo ... Full text Cite

Genetic control of the error-prone repair of a chromosomal double-strand break with 5' overhangs in yeast.

Journal article Genetics · August 2023 A targeted double-strand break introduced into the genome of Saccharomyces cerevisiae is repaired by the relatively error-prone nonhomologous end joining (NHEJ) pathway when homologous recombination is not an option. A zinc finger nuclease cleavage site wa ... Full text Cite

Spontaneous deamination of cytosine to uracil is biased to the non-transcribed DNA strand in yeast.

Journal article DNA Repair (Amst) · June 2023 Transcription in Saccharomyces cerevisiae is associated with elevated mutation and this partially reflects enhanced damage of the corresponding DNA. Spontaneous deamination of cytosine to uracil leads to CG>TA mutations that provide a strand-specific read- ... Full text Open Access Link to item Cite

Mutagenic repair of a ZFN-induced double-strand break in yeast: Effects of cleavage site sequence and spacer size.

Journal article DNA Repair (Amst) · December 2021 Double-strand breaks are repaired by error-free homologous recombination or by relatively error-prone pathways that directly join broken ends. Both types of repair have been extensively studied in Saccharomyces cerevisiae using enzymes HO or I-SceI, which ... Full text Link to item Cite

Trapped topoisomerase II initiates formation of de novo duplications via the nonhomologous end-joining pathway in yeast.

Journal article Proc Natl Acad Sci U S A · October 27, 2020 Topoisomerase II (Top2) is an essential enzyme that resolves catenanes between sister chromatids as well as supercoils associated with the over- or under-winding of duplex DNA. Top2 alters DNA topology by making a double-strand break (DSB) in DNA and passi ... Full text Open Access Link to item Cite

Recombinational Repair of Nuclease-Generated Mitotic Double-Strand Breaks with Different End Structures in Yeast.

Journal article G3 (Bethesda) · October 5, 2020 Mitotic recombination is the predominant mechanism for repairing double-strand breaks in Saccharomyces cerevisiae Current recombination models are largely based on studies utilizing the enzyme I-SceI or HO to create a site-specific break, each of which gen ... Full text Open Access Link to item Cite

The RBMX gene as a candidate for the Shashi X-linked intellectual disability syndrome.

Journal article Clin Genet · October 2015 A novel X-linked intellectual disability (XLID) syndrome with moderate intellectual disability and distinguishing craniofacial dysmorphisms had been previously mapped to the Xq26-q27 interval. On whole exome sequencing in the large family originally report ... Full text Link to item Cite