PubMed · 8924999
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E Streiblová, J Hasek. 1996. Light microscopy methods.. https://doi.org/10.1385/0-89603-319-8%3A383
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In this issue of Cell Genomics, McKeever et al.1 generate a single-nucleus transcriptomic atlas of ALS/FTLD brain and reveal widespread alternative polyadenylation changes. Their findings highlight 3' end RNA processing as a central integrator of stress responses, cell-type specificity, and disease susceptibility, offering new mechanistic insight and potential therapeutic directions.
It is currently well established that HIV-1 Vpr augments viral replication in primary human macrophages. In its virion-associated form, Vpr has been suggested to aid efficient translocation of the proviral DNA into the cell nucleus. Although Vpr growth-arrests dividing T cells, the relevance of this biological activity in nondividing macrophages is unclear. Here we use Vpr-mutants to demonstrate that the molecular determinants involved in G2-arresting T cells are also involved in increasing viral transcription in macrophages, even though these cells are refractive to the diploid DNA status typical of G2 phase. Our results suggest that the two phenotypes, namely the nuclear localization and the G2-arrest activity of the protein, segregate functionally among the late and early functions of Vpr. The nuclear localization property of Vpr correlates with its ability to effectively target the proviral DNA to the cell nucleus early in the infection, whereas the G2-arrest phenotype correlates with its ability to activate viral transcription after establishment of an infection. These two functions may render Vpr's role essential and not accessory under infection conditions that closely mimic the in vivo situation, that is, primary cells being infected at low viral inputs.
The possible existence in eukaryotic cells of an internal, non-chromatin nuclear structural framework that facilitates gene readout as a set of spatially concerted reactions has become a popular but controversial theater of investigation. This article endeavors to present a circumspect review of the nuclear matrix concept as we presently know it, framed around two contrasting hypotheses: (1) that an internal nuclear framework actively enhances gene expression (in much the same way the cytoskeleton mediates cell locomotion, mitosis and intracellular vesicular traffic) versus (2) that the interphase chromosomes have fixed, inherited positions and that the DNA replication, transcripton and RNA processing machinery diffusionally arrives at sites of gene readout, with some aspects of nuclear structure thus being more a result than a cause of gene expression. On balance, the available information suggests that interactions among various gene expression machines may contribute to isolated nuclear matrix preparations. Some components of isolated nuclear matrix preparations may also reflect induced or reconfigured protein-protein associations. The protein characterization and ultrastructural analysis of the isolated nuclear matrix has advanced significantly in recent years, although controversies remain. Important new clues are now coming in from promising contemporary lines of research that report on nuclear structure in living cells.