Comparative molecular genetic analysis of simian and human HIV-1 integrase interactor INI1/SMARCB1/SNF5

Pyeon, Dohun; Price, Lenore; Park, In-Woo

doi:10.1007/s00705-015-2585-x

Cited by 4 publications

(5 citation statements)

References 11 publications

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“…SMARCB1 is known to inhibit HIV replication in cell lines, possibly through the stabilization of pre-intregration complexes in non-reactive conformations (Das et al, 2009; Maroun et al, 2006; Pyeon et al, 2015). XRCC6 (Ku70) and other components of the NHEJ pathway, however, have an unclear role in the HIV lifecycle, though some results suggest a role in post-integration expression (Baekelandt et al, 2000; Jeanson et al, 2002; Li et al, 2001; Manic et al, 2013).…”

Section: Resultsmentioning

confidence: 99%

A Cas9 Ribonucleoprotein Platform for Functional Genetic Studies of HIV-Host Interactions in Primary Human T Cells

et al. 2016

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SUMMARY New genetic tools are needed to understand the functional interactions between HIV and human host factors in primary cells. We recently developed a method to edit the genome of primary CD4+ T cells by electroporation of CRISPR/Cas9 ribonucleoproteins (RNPs). Here, we adapted this methodology to a high-throughput platform for the efficient, arrayed editing of candidate host factors. CXCR4 or CCR5 knock-out cells generated with this method are resistant to HIV infection in a tropism-dependent manner, whereas knock-out of LEDGF or TNPO3 results in a tropism-independent reduction in infection. CRISPR/Cas9 RNPs can furthermore edit multiple genes simultaneously, enabling studies of interactions among multiple host and viral factors. Finally, in an arrayed screen of 45 genes associated with HIV integrase, we identified several candidate dependency/restriction factors, demonstrating the power of this approach as a discovery platform. This technology should accelerate target validation for pharmaceutical and cell-based therapies to cure HIV infection.

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Section: Resultsmentioning

confidence: 99%

A Cas9 Ribonucleoprotein Platform for Functional Genetic Studies of HIV-Host Interactions in Primary Human T Cells

et al. 2016

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“…Among them, we particularly focused on Smarcb1, a sub-hub gene encoding an SWI/SNF-related matrix-associated actin-dependent regulator. It has seven isoforms in mouse and two in human, and this gene was previously reported to be related to chromatin remodeling [30][31][32]. Exon counts showed that most of the AS events occurred at exons 7-9,13-27, and 23-27, the latter of which correspond to the 3′ end of the CDS of SMARCB1 (Fig.…”

Section: Alternative Splicing At the Two-cell Stagementioning

confidence: 86%

Alternative splicing signatures in preimplantation embryo development

Tian¹,

Li²,

Wu³

2020

Cell Biosci

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Background: Preimplantation embryo development is a highly ordered sequence of processes and it requires a precise temporal and spatial control of gene expression. Alternative splicing (AS) is a crucial process that changes the genomic instructions into functional proteins, playing a critical role in the regulation of gene expression. Therefore, studies of AS can significantly improve our understanding of transcription and splicing events in preimplantation embryo development. Results: To study signatures of AS in embryo development, we firstly identified the critical stage for gene transcription during the preimplantation embryo development. By analyzing single cells RNA-seq (scRNA-seq) data, we found that the two-cell stage is a critical stage for gene transcription in preimplantation embryo development. Further study showed that AS was widespread in preimplantation embryo development, especially at the two-cell stage. In combination with high-throughput chromosome conformation (Hi-C) data, we demonstrated that AS genes were highly enriched in TAD boundaries, while they had no relationship with the A/B compartment and TAD. Conclusion: Our results provide new insight into the relationship among AS, gene transcription and chromatin structure in preimplantation embryo development.

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“…The functions of these two isoforms have not been characterized, but one paper reported that the longer isoform seems to be more common in no‐fetal tissues while a shorter form is more prevalent in fetal tissues 91 . Interestingly, this two‐isoform pattern is also observed among humans, mice, and simian 92 . Moreover, the SFH1 in Saccharomyces cerevisiae , SNR1 in Drosophilia , SNF5 in Caenorhabditis elegans , and yeast counterparts have three highly conserved regions 89 .…”

Section: Mechanisms Of Mutated Swi/snf Complex In Tumorigenesismentioning

confidence: 99%

“… 91 Interestingly, this two‐isoform pattern is also observed among humans, mice, and simian. 92 Moreover, the SFH1 in Saccharomyces cerevisiae , SNR1 in Drosophilia , SNF5 in Caenorhabditis elegans , and yeast counterparts have three highly conserved regions. 89 Two of the three conserved regions are imperfect repeat motifs, Repeat 1(amino acids 186–245) and Repeat 2 (amino acids 259–319) (Figure 2B ).…”

Section: Mechanisms Of Mutated Swi / Snf...mentioning

confidence: 99%

Recent insights into the SWI/SNF complex and the molecular mechanism of hSNF5 deficiency in rhabdoid tumors

et al. 2023

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Genetic information encoded by DNA is packaged in the nucleus using the chromatin structure. The accessibility of transcriptional elements in DNA is controlled by the dynamic structural changes of chromatin for the appropriate regulation of gene transcription. Chromatin structure is regulated by two general mechanisms, one is histone modification and the other is chromatin remodeling in an ATP‐dependent manner. Switch/sucrose nonfermentable (SWI/SNF) complexes utilize the energy from ATP hydrolysis to mobilize nucleosomes and remodel the chromatin structure, contributing to conformational changes in chromatin. Recently, the inactivation of encoding genes for subunits of the SWI/SNF complexes has been documented in a series of human cancers, accounting for up to almost 20% of all human cancers. For example, human SNF5 (hSNF5), the gene that encodes a subunit of the SWI/SNF complexes, is the sole mutation target that drives malignant rhabdoid tumors (MRT). Despite remarkably simple genomes, the MRT has highly malignant characteristics. As a key to understanding MRT tumorigenesis, it is necessary to fully examine the mechanism of chromatin remodeling by the SWI/SNF complexes. Herein, we review the current understanding of chromatin remodeling by focusing on SWI/SNF complexes. In addition, we describe the molecular mechanisms and influences of hSNF5 deficiency in rhabdoid tumors and the prospects for developing new therapeutic targets to overcome the epigenetic drive of cancer that is caused by abnormal chromatin remodeling.

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Comparative molecular genetic analysis of simian and human HIV-1 integrase interactor INI1/SMARCB1/SNF5

Cited by 4 publications

References 11 publications

A Cas9 Ribonucleoprotein Platform for Functional Genetic Studies of HIV-Host Interactions in Primary Human T Cells

A Cas9 Ribonucleoprotein Platform for Functional Genetic Studies of HIV-Host Interactions in Primary Human T Cells

Alternative splicing signatures in preimplantation embryo development

Recent insights into the SWI/SNF complex and the molecular mechanism of hSNF5 deficiency in rhabdoid tumors

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