| 2003 |
TAF7L is a germ-cell-specific paralogue of TFIID subunit TAF7; biochemical experiments show that a subpopulation of TAF7L is tightly associated with TBP in pachytene and haploid cells, and TAF7L physically interacts with TFIID subunit TAF1. Its intracellular localization shifts dynamically from cytoplasmic in spermatogonia/early spermatocytes to nuclear in late pachytene spermatocytes and round spermatids, coinciding with decreased TAF7 expression and increased nuclear TBP, indicating TAF7L replaces TAF7 as a TFIID subunit during male germ-cell differentiation. |
Biochemical co-association assays (TAF7L with TBP and TAF1), immunofluorescence/subcellular fractionation for localization, western blot for expression timing |
Journal of cell science |
Medium |
12665565
|
| 2007 |
Loss of Taf7l in mice (knockout by homologous recombination/Cre-loxP) causes reduced testis weight, sharply reduced sperm count, abnormal sperm morphology (folded tails), and reduced sperm motility. Microarray profiling revealed ≥2-fold reduction in six transcripts in mutant testes, including Fscn1 (an F-actin-bundling protein), indicating TAF7L has a gene-selective role in transcription during male germ-cell differentiation. |
Homologous recombination knockout mouse, histology, sperm morphology/motility analysis, microarray expression profiling |
Molecular and cellular biology |
High |
17242199
|
| 2013 |
TAF7L cooperates with TRF2 to regulate postmeiotic spermiogenic genes: TAF7L physically associates with TRF2 both in vitro and in testis (biochemical studies); ChIP-seq shows TAF7L binds to promoters of activated postmeiotic genes; Taf7l KO mice develop postmeiotic arrest at the first stage of spermiogenesis, phenotypically similar to Trf2−/− mice. TAF7L and TRF2 co-regulate a subset of postmeiotic genes but not Taf4b-regulated germ stem cell genes. |
In vitro binding assays, co-immunoprecipitation in testis, genome-wide ChIP-seq, mRNA-seq expression profiling, loss-of-function mouse model (backcrossed to N9), histological analysis, genetic epistasis with Trf2 and Taf4b knockouts |
Proceedings of the National Academy of Sciences of the United States of America |
High |
24082143
|
| 2013 |
TAF7L plays a dual role in adipocyte differentiation: (1) it interacts with PPARγ at enhancers as a transcriptional cofactor, and (2) it interacts with TBP/Pol II at core promoters as a component of the core transcriptional machinery. In vitro binding studies confirmed TAF7L forms complexes with both TBP and PPARγ. Depletion of TAF7L reduces adipocyte-specific gene expression and compromises adipocyte differentiation and white adipose tissue development; ectopic expression in myoblasts reprograms them into adipocytes upon induction. |
In vitro binding assays (TAF7L with TBP and PPARγ), mRNA-seq expression profiling, ChIP-seq, siRNA depletion, ectopic expression/reprogramming assay in myoblasts |
eLife |
High |
23326641
|
| 2014 |
TAF7L acts as a molecular switch between brown adipose tissue and muscle lineages. In adipose tissue, TAF7L-containing TFIID complexes associate with PPARγ to mediate DNA looping between distal enhancers and core promoter elements, promoting BAT lineage specification. |
In vivo and in vitro lineage analysis, chromatin conformation/looping assays, co-association studies of TAF7L-TFIID with PPARγ, loss-of-function and gain-of-function experiments |
eLife |
Medium |
24876128
|
| 2020 |
BNC1 physically associates with TAF7L both in vitro and in testis (biochemical analysis), and the BNC1/TAF7L complex undergoes nuclear translocation to regulate spermatogenesis-specific gene promoters. A truncation mutation in BNC1 disables nuclear translocation of the BNC1/TAF7L complex, disturbing expression of spermatogenesis genes (Klhl10, Tex14, Spatc1) and leading to testicular premature aging. |
Co-immunoprecipitation/in vitro binding, ChIP-seq, genome-wide expression profiling, truncation mutation mouse model, immunofluorescence for nuclear translocation |
Journal of molecular cell biology |
Medium |
31065688
|
| 2022 |
A conserved aspartate residue (D136 in human TAF7L; equivalent D in yeast TAF7) is essential for function: genetic complementation experiments in budding yeast demonstrate that the conserved aspartate or analogous asparagine in yeast TAF7 is required for cell viability, and its mutation to glycine is lethal. The corresponding D144G substitution in mouse Taf7l alters transcriptomic profiles in testes (RNA-seq) without abolishing fertility, supporting the human D136G missense as a risk factor for oligozoospermia. |
Genetic complementation in yeast (cell viability assay), knock-in mouse model (D144G), RNA-seq of mutant testes |
Biology of reproduction |
Medium |
35554494
|
| 2023 |
Deleterious frameshift and missense variants in TAF7L (including truncating variants c.1301_1302del, c.508delA, c.719dupA and missense c.699G>T) cause oligoasthenoteratozoospermia in men. In vitro studies show these mutations impair histone-to-protamine exchange and chromatin compaction in sperm heads. The truncating variant 719dupA produces a nuclear-retained truncated TAF7L protein, while other frameshift variants abolish detectable TAF7L protein expression. |
Whole-exome sequencing, Western blotting and immunocytochemistry for protein localization/expression, transmission electron microscopy, in vitro fertilization assay (ICSI) |
Frontiers in endocrinology |
Medium |
36714566
|
| 2024 |
In rat, TAF7L is prominently expressed in preleptotene-to-leptotene spermatocytes, and CRISPR/Cas9-mediated loss-of-function (110 bp deletion causing frameshift/premature stop in exon 3) causes male infertility due to meiotic arrest at late zygotene/early pachynema stages, with defects in sex body formation. This phenotype is more severe than in the Taf7l null mouse, demonstrating TAF7L is essential for early male germ cell development. |
CRISPR/Cas9 global knockout rat model, histology, immunofluorescence, germline transmission verification |
FASEB journal |
High |
38112167
|
| 2026 |
In dorsal root ganglion (DRG) neurons, TAF7L expression is induced after peripheral nerve injury (>5-fold by day 14 post-injury). Lentiviral knockdown of Taf7l reduces neurite length by 27% without affecting initiation rate, while Taf7l overexpression increases both initiation rate and axonal length, demonstrating TAF7L functions as a transcriptional regulator promoting neurite outgrowth in the peripheral nervous system. |
Genome-wide expression profiling (correlation with neurite outgrowth), immunohistochemistry, quantitative RT-PCR (injury time course), lentiviral knockdown and overexpression in DRG neurons, neurite outgrowth assay |
Neuroscience letters |
Medium |
41730469
|