The myopathic transcription factor DUX4 induces discordant dysregulation of transcript and protein levels, demonstrating a key role for post-transcriptional gene regulation in facioscapulohumeral muscular dystrophy.
Post-translational modification of histone H3K36 is not required to suppress cryptic transcription initiation or to include alternative exons in Drosophila; instead it promotes expression of active genes by stimulating polyadenylation.
The human leukemia virus HTLV-1 causes abnormal chromatin looping in tens of thousands of infected T cell clones in each host, and abnormal host transcription both flanking the integrated provirus and at distant loci in cis.
Bacteria use the transcription factor binding region of their transcription activator-like effectors to hijack host basal transcription factor to cause rice diseases by activating host susceptibility genes.
Herpes simplex ICP4 preferentially binds to and delineates the viral genome, ultimately resulting in robust viral transcription at the expense of the host.
The unspliced HAC1 mRNA does not give rise to detectable protein in budding yeast, despite its cytoplasmic localization, due to a two-part post-transcriptional silencing mechanism.
Mass spectrometry exposes a post-transcriptionally regulated reduction in protein diversity in hematopoietic stem cells, including a lack of detectable Dnmt3a protein levels despite mRNA levels comparable to progenitors.
Genome-wide measurements on mouse liver cells show that transcription, and a particular key transcription factor, have a smaller than expected influence on the mouse circadian system.
