Chromatin disruption in the promoter of Bovine Leukemia Virus during transcriptional activation

Bovine leukemia virus expression relies on its chromatin organization after integration into the host cell genome. Proviral latency, which results from transcriptional repression in vivo, represents a viral strategy to escape the host immune system and likely allows for tumor progression. Here, we discriminated two types of latency: an easily reactivable latent state of the YR2 provirus and a ‘locked’ latent state of the L267 provirus. The defective YR2 provirus was characterized by the presence of nuclease hypersensitive sites at the U3/R junction and in the R/U5 region of the 5′-long terminal repeat (5′-LTR), whereas the L267 provirus displayed a closed chromatin configuration at the U3/R junction. Reactivation of viral expression in YR2 cells by the phorbol 12-myristate 13-acetate (PMA) plus ionomycin combination was accompanied by a rapid but transient chromatin remodeling in the 5′-LTR, leading to an increased PU.1 and USF-1/USF-2 recruitment in vivo sustained by PMA/ionomycin-mediated USF phosphorylation. In contrast, viral expression was not reactivated by PMA/ionomycin in L267 cells, because the 5′-LTR U3/R region remained inaccessible to nucleases and hypermethylated at CpG dinucleotides. Remarkably, we elucidated the BLV 5′-LTR chromatin organization in PBMCs isolated from BLV-infected cows, thereby depicting the virus hiding in vivo in its natural host

Etude de la régulation transcriptionnelle du virus de la leucémie bovine: rôle de la chromatine et des facteurs de transcription PU.1 et Sp1/Sp3

Doctorat en Sciencesinfo:eu-repo/semantics/nonPublishe

Body size in the ant-associated isopod Platyarthrus hoffmannseggii is host-dependent

Many symbionts live in association with different species. It can be expected that these distinct hosts might have a different effect on key life-history traits of the associated symbionts. Here, we compared the key trait body size of the obligatorily ant-associated isopod Platyarthrus hoffmannseggii collected in nests of two types of sympatric ant hosts. This isopod species showed surprisingly large differences in body size depending on type of host ant, with the head width of females and males associated with organic mound building red wood ants (RWAs) being, respectively, 1.30 and 1.17 times larger than isopods sympatrically living in earth nests of Lasius flavus. There was also a higher proportion of females in many RWA nests, but this pattern was not consistent across all nests. Genetic analyses and aggression trials did not reveal cryptic groups specialized to different hosts. Therefore, we argue that the isopods exhibit size plasticity because of different host nest conditions. Absence of host aggression and optimal abiotic conditions in RWA nests might promote a larger isopod body size. Overall, this study shows that the association of a symbiont with different hosts might induce phenotypic plasticity in a symbiont key trait

A pervasive role of histone acetyltransferases and deacetylases in an NF-kappaB-signaling code.

Most nuclear factor-kappaB (NF-kappaB) inducers converge to activate the IkappaB kinase (IKK) complex, leading to NF-kappaB nuclear accumulation. However, depending on the inducer and the cell line, the subset of NF-kappaB-induced genes is different, underlining a complex regulation network. Recent findings have begun to delineate that histone and non-histone protein acetylation is involved, directly and indirectly, in controlling the duration, strength and specificity of the NF-kappaB-activating signaling pathway at multiple levels. Acetylation and deacetylation events, in combination with other post-translational protein modifications, generate an 'NF-kappaB-signaling code' and regulate NF-kappaB-dependent gene transcription in an inducer- and promoter-dependent manner. Indeed, the intricate involvement of histone acetyltransferases and histone deacetylases modulates both the NF-kappaB-signaling pathway and the transcriptional transactivation of NF-kappaB-dependent genes.Journal ArticleResearch Support, Non-U.S. Gov'tReviewinfo:eu-repo/semantics/publishe

Chromatin disruption in the promoter of Bovine Leukemia Virus during transcriptional activation

info:eu-repo/semantics/publishe

Identification and characterization of a PU.1/Spi-B binding site in the bovine leukemia virus long terminal repeat.

Bovine leukemia virus (BLV) is a B-lymphotropic oncogenic retrovirus whose transcriptional promoter is located in the viral 5' long terminal repeat (LTR). To date, no B-lymphocyte-specific cis-regulatory element has been identified in this region. Since ETS proteins are known to regulate transcription of numerous retroviruses, we searched for the presence in the BLV promoter region of binding sites for PU.1/Spi-1, a B-cell- and macrophage-specific ETS family member. In this report, nucleotide sequence analysis of the viral LTR identified a PUbox located at -95/-84 bp. We demonstrated by gel shift and supershift assays that PU.1 and the related Ets transcription factor Spi-B interacted specifically with this PUbox. A 2-bp mutation (GGAA-->CCAA) within this motif abrogated PU.1/Spi-B binding. This mutation caused a marked decrease in LTR-driven basal gene expression in transient transfection assays of B-lymphoid cell lines, but did not impair the responsiveness of the BLV promoter to the virus-encoded transactivator Tax(BLV). Moreover, ectopically expressed PU.1 and Spi-B proteins transactivated the BLV promoter in a PUbox-dependent manner. Taken together, our results provide the first demonstration of regulation of the BLV promoter by two B-cell-specific Ets transcription factors, PU.1 and Spi-B. The PU.1/Spi-B binding site identified here could play an important role in BLV replication and B-lymphoid tropism.In VitroJournal ArticleResearch Support, Non-U.S. Gov'tinfo:eu-repo/semantics/publishe

Identification and characterization of a PU.1/Spi-B binding site in the bovine leukemia virus long terminal repeat

info:eu-repo/semantics/publishe

Role of the transcription factor PU.1 and role of chromatin organization in the transcriptional regulation of the Bovine Leukemia Virus (BLV)

info:eu-repo/semantics/publishe