Top 7 Biorxiv Papers Today in Molecular Biology


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#1. Tagsteady: a metabarcoding library preparation protocol to avoid false assignment of sequences to samples
Christian Caroe, Kristine Bohmann
Metabarcoding of environmental DNA (eDNA) and DNA extracted from bulk specimen samples is a powerful tool in studies of biodiversity, diet and ecological interactions as its inherent labelling of amplicons allows sequencing of taxonomically informative genetic markers from many samples in parallel. However, the occurrence of so-called ′tag-jumps′ can cause incorrect assignment of sequences to samples and artificially inflate diversity. Two steps during library preparation of pools of 5′ nucleotide-tagged amplicons have been suggested to cause tag-jumps; i) T4 DNA polymerase blunt-ending in the end-repair step and ii) post-ligation PCR amplification of amplicon libraries. The discovery of tag-jumps has led to recommendations to only carry out metabarcoding PCR amplifications with primers carrying twin-tags to ensure that tag-jumps cannot result in false assignments of sequences to samples. As this increases both cost and workload, a metabarcoding library preparation protocol which circumvents the two steps that causes tag-jumps is...
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Authors: 2
Total Words: 9440
Unqiue Words: 2636

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#2. A Fob1 independent role for the Smc5/6 complex in the rDNA that modulates lifespan.
Sarah Moradi Fard, Aditya Mojumdar, Megan Chan, Troy Anthony Alan Harkness, Jennifer A Cobb
The ribosomal DNA (rDNA) in Saccharomyces cerevisiae is in one tandem repeat array on Chromosome XII. Two spacer regions within each repetitive element, called non- transcribed spacer 1 (NTS1) and NTS2, are important in nucleolar organization. Smc5/6 localizes to both NTS1 and NTS2 and is involved in the regulation of Sir2 and Cohibin binding at NTS1, whereas Fob1 and Sir2 are required for optimal binding of the complex to NTS1 and NTS2, respectively. We demonstrate that Smc5/6 functions in chromatin silencing at NTS1 independently of its role in homologous recombination (HR) when forks pause at the replication fork barrier (RFB). In contrast, when the complex does not localize to the rDNA in nse3-1 mutants, the shortened lifespan correlates with NTS2 homeostasis independently of FOB1 status. Our data identify the importance of Smc5/6 integrity in NTS2 transcriptional silencing and repeat tethering, which in turn underscores rDNA stability and replicative lifespan.
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biorxivpreprint: A Fob1 independent role for the Smc5/6 complex in the rDNA that modulates lifespan. https://t.co/UDDxmCQtUr #bioRxiv
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#3. METTL4 catalyzes m6Am methylation in U2 snRNA to regulate pre-mRNA splicing
Yeek Teck Goh, Casslynn W. Q. Koh, Donald Yuhui Sim, Xavier Roca, Wee Siong Sho Goh
N6-methylation of 2′-O-methyladenosine (Am) in RNA occurs in eukaryotic cells to generate N6,2′-O-dimethyladenosine (m6Am). Identification of the methyltransferase responsible for m6Am catalysis has accelerated studies on the function of m6Am in RNA processing. While m6Am is generally found in the first transcribed nucleotide of mRNAs, the modification is also found internally within U2 snRNA. However, the writer required for catalyzing internal m6Am formation had remained elusive. By sequencing transcriptome-wide RNA methylation at single-base-resolution, we identified human METTL4 as the writer that directly methylates Am at U2 snRNA position 30 into m6Am. We found that METTL4 localizes to the nucleus and its conserved methyltransferase catalytic site is required for U2 snRNA methylation. By sequencing human cells with overexpressed Mettl4, we determined METTL4′s in vivo target RNA motif specificity. In the absence of Mettl4 in human cells, U2 snRNA lacks m6Am thereby affecting a subset of splicing events that exhibit specific...
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nickschurch: RT @biorxivpreprint: METTL4 catalyzes m6Am methylation in U2 snRNA to regulate pre-mRNA splicing https://t.co/a3TV4yWndJ #bioRxiv
ShoGohLab: RT @biorxivpreprint: METTL4 catalyzes m6Am methylation in U2 snRNA to regulate pre-mRNA splicing https://t.co/a3TV4yWndJ #bioRxiv
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Total Words: 0
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#4. Macrophages Promote Aortic Valve Cell Calcification Through STAT3 Splicing
Michael Raddatz, Tessa Huffstater, Matthew R Bersi, Bradley Reinfeld, Matthew Madden, Sabrina Booton, Kimryn Rathmell, Jeffrey C Rathmell, Brian Lindman, Meena Madhur, W. David Merryman
Objective Macrophages have been described in calcific aortic valve disease, but it is unclear if they promote or counteract calcification. We aimed to determine how macrophages are involved in calcification using the Notch1+/- model of calcific aortic valve disease. Approach and Results Macrophages in wild-type and Notch1+/- murine aortic valves were characterized by flow cytometry. Macrophages in Notch1+/- aortic valves had increased expression of MHCII. We then used bone marrow transplants to test if differences in Notch1+/- macrophages drive disease. Notch1+/- mice had increased valve thickness, macrophage infiltration, and M1-like macrophage polarization regardless of transplanted bone marrow genotype. In vitro approaches confirm that Notch1+/- aortic valve cells promote macrophage invasion as quantified by migration index and M1-like polarization quantified by Ly6C and CCR2 positivity regardless of macrophage genotype. Finally, we found that macrophage interaction with aortic valve cells promotes osteogenic, but not...
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biorxivpreprint: Macrophages Promote Aortic Valve Cell Calcification Through STAT3 Splicing https://t.co/X6U5F6ZRur #bioRxiv
AlexSilverMSTP: RT @biorxivpreprint: Macrophages Promote Aortic Valve Cell Calcification Through STAT3 Splicing https://t.co/X6U5F6ZRur #bioRxiv
MichaelR21: RT @biorxivpreprint: Macrophages Promote Aortic Valve Cell Calcification Through STAT3 Splicing https://t.co/X6U5F6ZRur #bioRxiv
MichaelR21: RT @biorxivpreprint: Macrophages Promote Aortic Valve Cell Calcification Through STAT3 Splicing https://t.co/X6U5F6ZRur #bioRxiv
enerphyschem: RT @biorxivpreprint: Macrophages Promote Aortic Valve Cell Calcification Through STAT3 Splicing https://t.co/X6U5F6ZRur #bioRxiv
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Authors: 11
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#5. Interleukin-35 pretreatment attenuates lipopolysaccharide-induced heart injury by inhibition of inflammation, apoptosis and fibrosis
Yang Fu, Huan Hu, Meng Li, Huasong Xia, Yue Liu, Xiaopei Sun, Yang Hu, Fulin Song, Xiaoshu Cheng, Ping Li, Yanqing Wu
Previous studies have demonstrated that targeting inflammation is a promising strategy for treating lipopolysaccharide (LPS)-induced sepsis and related heart injury. Interleukin-35 (IL-35), which consists of two subunits, Epstein-Barr virus-induced gene 3 (EBI3) and p35, is an immunosuppressive cytokine of the IL-12 family and exhibits strong anti-inflammatory activity. However, the role of IL-35 in LPS-induced heart injury remains obscure. In this study, we explored the role of IL-35 in heart injury induced by LPS and its potential mechanisms. Mice were treated with a plasmid-encoding IL-35 (pIL-35) and then injected intraperitoneally (ip) with LPS (10 mg/kg). Cardiac function was assessed by echocardiography 12 h later. LPS apparently decreased the expression of EBI3 and p35 and caused cardiac dysfunction and pathological changes, which were significantly improved by pIL-35 pretreatment. Moreover, pIL-35 pretreatment significantly decreased the levels of cardiac proinflammatory cytokines including TNF-α, IL-6, and IL-1β, and the...
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biorxivpreprint: Interleukin-35 pretreatment attenuates lipopolysaccharide-induced heart injury by inhibition of inflammation, apoptosis and fibrosis https://t.co/zdcBvX8E3d #bioRxiv
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Authors: 11
Total Words: 7857
Unqiue Words: 2240

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#6. Transcriptional analysis supports the expression of human snRNA variants and reveals U2 snRNA homeostasis by an abundant U2 variant
Brian Kosmyna, Varun Gupta, Charles C Query
Although expansion of snRNA genes in the human genome and sequence variation in expressed transcripts were both identified long ago, no study has comprehensively analyzed which genes are transcriptionally active. Here, we use comprehensive bioinformatic analysis to differentiate between similar or identical genomic loci to determine that 49 snRNA genes are actively transcribed. This greatly expands on previous observation of sequence variation within snRNA transcripts. Further analysis of U2 snRNA variants reveals sequence variation maintains conserved secondary structures, yet sensitizes these U2 snRNAs to modulation of assembly factors. Homeostasis of total U2 snRNA level is maintained by altering the ratio of canonical and an abundant U2 snRNA variant. Both canonical and variant snRNA promoters respond to MYC and appear differentially sensitive to increased MYC levels. Thus, we identify transcribed snRNA variants and the sequence variation within, and propose mechanisms of transcriptional and posttranscriptional regulation of...
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Authors: 3
Total Words: 15236
Unqiue Words: 3718

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#7. NF90 Modulates Processing of a Subset of Human Pri-miRNAs
Giuseppa Grasso, Takuma Higuchi, Jerome Barbier, Marion Helsmoortel, Claudio Lorenzi, Gabriel Sanchez, Maxime Bello, William Ritchie, Shuji Sakamoto, Rosemary Kiernan
MicroRNAs are predicted to regulate the expression of more than 60% of mammalian genes and play fundamental roles in most biological processes. Deregulation of miRNA expression is a hallmark of most cancers and further investigation of mechanisms controlling miRNA biogenesis is needed. The dsRNA-binding protein, NF90 has been shown to act as a competitor of Microprocessor for a limited number of pri-miRNAs. Here, we show that NF90 has a more widespread effect on pri-miRNA biogenesis than previously thought. Genome-wide approaches revealed that NF90 is associated with the stem region of 38 pri-miRNAs, in a manner that is largely exclusive of Microprocessor. Following loss of NF90, 22 NF90-bound pri-miRNAs showed increased abundance of mature miRNA products. NF90-targeted pri-miRNAs are highly stable, having a lower free energy and fewer mismatches compared to all pri-miRNAs. Mutations leading to less stable structures reduced NF90 binding while increasing pri-miRNA stability led to acquisition of NF90 association, as determined by...
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biorxivpreprint: NF90 Modulates Processing of a Subset of Human Pri-miRNAs https://t.co/o99jIj3utJ #bioRxiv
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Authors: 10
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