| First Author | Mielnicka M | Year | 2024 |
| Journal | Life Sci Alliance | Volume | 7 |
| Issue | 7 | PubMed ID | 38719749 |
| Mgi Jnum | J:349240 | Mgi Id | MGI:7639037 |
| Doi | 10.26508/lsa.202302512 | Citation | Mielnicka M, et al. (2024) Trim66's paternal deficiency causes intrauterine overgrowth. Life Sci Alliance 7(7) |
| abstractText | The tripartite motif-containing protein 66 (TRIM66, also known as TIF1-delta) is a PHD-Bromo-containing protein primarily expressed in post-meiotic male germ cells known as spermatids. Biophysical assays showed that the TRIM66 PHD-Bromodomain binds to H3 N-terminus only when lysine 4 is unmethylated. We addressed TRIM66's role in reproduction by loss-of-function genetics in the mouse. Males homozygous for Trim66-null mutations produced functional spermatozoa. Round spermatids lacking TRIM66 up-regulated a network of genes involved in histone acetylation and H3K4 methylation. Profiling of H3K4me3 patterns in the sperm produced by the Trim66-null mutant showed minor alterations below statistical significance. Unexpectedly, Trim66-null males, but not females, sired pups overweight at birth, hence revealing that Trim66 mutations cause a paternal effect phenotype. |
