Publications by authors named "Archana B Prusty"

Article Synopsis
  • RNA helicases are important for maintaining RNA levels in cells and are linked to diseases, such as SMARD1, which is associated with the IGHMBP2 protein.* -
  • IGHMBP2 helps in translating specific mRNAs by preventing ribosome stalling, which is crucial for synthesizing proteins involved in the THO complex, important for mRNA production and export.* -
  • Problems with IGHMBP2 regulation can disrupt cellular processes and may play a role in the development of SMARD1, highlighting potential targets for new treatments.*
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Spliceosomal snRNPs are multicomponent particles that undergo a complex maturation pathway. Human Sm-class snRNAs are generated as 3'-end extended precursors, which are exported to the cytoplasm and assembled together with Sm proteins into core RNPs by the SMN complex. Here, we provide evidence that these pre-snRNA substrates contain compact, evolutionarily conserved secondary structures that overlap with the Sm binding site.

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Herpesviruses have mastered host cell modulation and immune evasion to augment productive infection, life-long latency and reactivation. A long appreciated, yet undefined relationship exists between the lytic-latent switch and viral non-coding RNAs. Here we identify viral microRNA (miRNA)-mediated inhibition of host miRNA processing as a cellular mechanism that human herpesvirus 6A (HHV-6A) exploits to disrupt mitochondrial architecture, evade intrinsic host defences and drive the switch from latent to lytic virus infection.

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The activity of the SMN complex in promoting the assembly of pre-mRNA processing UsnRNPs correlates with condensation of the complex in nuclear Cajal bodies. While mechanistic details of its activity have been elucidated, the molecular basis for condensation remains unclear. High SMN complex phosphorylation suggests extensive regulation.

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Article Synopsis
  • A mutation in the SNRPE gene, linked to pre-mRNA processing, has been identified in a patient with congenital microcephaly and intellectual disability.
  • This mutation disrupts the normal function of the SmE protein, preventing it from interacting with the SMN complex and forming U snRNPs, leading to significant mRNA splicing errors in patient-derived cells.
  • The study indicates that these splicing defects, particularly affecting the EMX2 mRNA crucial for brain development, may contribute to the neurological issues associated with microcephaly.
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Specialized assembly factors facilitate the formation of many macromolecular complexes in vivo. The formation of Sm core structures of spliceosomal U-rich small nuclear ribonucleoprotein particles (UsnRNPs) requires assembly factors united in protein arginine methyltransferase 5 (PRMT5) and survival motor neuron (SMN) complexes. We demonstrate that perturbations of this assembly machinery trigger complex cellular responses that prevent aggregation of unassembled Sm proteins.

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The Polycomb repressive complex 2 (PRC2) confers transcriptional repression through histone H3 lysine 27 trimethylation (H3K27me3). Here, we examined how PRC2 is modulated by histone modifications associated with transcriptionally active chromatin. We provide the molecular basis of histone H3 N terminus recognition by the PRC2 Nurf55-Su(z)12 submodule.

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