The Subread aligner: fast, accurate and scalable read mapping by seed-and-vote

Liao, Yang; Smyth, Gordon K.; Shi, Wei

doi:10.1093/nar/gkt214

Cited by 2,352 publications

(1,771 citation statements)

References 50 publications

Supporting

Mentioning

1,770

Contrasting

Unclassified

Order By: Relevance

“…RNA-seq Reads were aligned to the GRCm38/mm10 build of the Mus musculus genome using the Subread aligner. 50 Only uniquely mapped reads were retained. Genewise counts were obtained using featureCounts.…”

Section: Methodsmentioning

confidence: 99%

A point mutation in the Ncr1 signal peptide impairs the development of innate lymphoid cell subsets

et al. 2018

Self Cite

View full text Add to dashboard Cite

NKp46 (CD335) is a surface receptor shared by both human and mouse natural killer (NK) cells and innate lymphoid cells (ILCs) that transduces activating signals necessary to eliminate virus-infected cells and tumors. Here, we describe a spontaneous point mutation of cysteine to arginine (C14R) in the signal peptide of the NKp46 protein in congenic Ly5.1 mice and the newly generated NCRB6C14R strain. Ly5.1C14R NK cells expressed similar levels of Ncr1 mRNA as C57BL/6, but showed impaired surface NKp46 and reduced ability to control melanoma tumors in vivo. Expression of the mutant NKp46C14R in 293T cells showed that NKp46 protein trafficking to the cell surface was compromised. Although Ly5.1C14R mice had normal number of NK cells, they showed an increased number of early maturation stage NK cells. CD49a+ILC1s were also increased but these cells lacked the expression of TRAIL. ILC3s that expressed NKp46 were not detectable and were not apparent when examined by T-bet expression. Thus, the C14R mutation reveals that NKp46 is important for NK cell and ILC differentiation, maturation and function.SignificanceInnate lymphoid cells (ILCs) play important roles in immune protection. Various subsets of ILCs express the activating receptor NKp46 which is capable of recognizing pathogen derived and tumor ligands and is necessary for immune protection. Here, we describe a spontaneous point mutation in the signal peptide of the NKp46 protein in congenic Ly5.1 mice which are widely used for tracking cells in vivo. This Ncr1 C14R mutation impairs NKp46 surface expression resulting in destabilization of Ncr1 and accumulation of NKp46 in the endoplasmic reticulum. Loss of stable NKp46 expression impaired the maturation of NKp46+ ILCs and altered the expression of TRAIL and T-bet in ILC1 and ILC3, respectively.

show abstract

Section: Methodsmentioning

confidence: 99%

A point mutation in the Ncr1 signal peptide impairs the development of innate lymphoid cell subsets

et al. 2018

Self Cite

View full text Add to dashboard Cite

show abstract

“…Sequencing reads were mapped against the Arabidopsis genome (TAIR version 10) using the subread software and default parameter (Liao et al, 2013), and sorted and indexed using the samtools software (Li et al, 2009). All subsequent analyses were performed in the statistical software R (R Core Team, 2015) and software packages implemented in the Bioconductor project (Gentleman et al, 2004).…”

Section: Analyses Of Rna-seq Datasetmentioning

confidence: 99%

Seed Production Affects Maternal Growth and Senescence in Arabidopsis

Wuest

Philipp²,

Guthörl³

et al. 2016

Plant Physiol.

View full text Add to dashboard Cite

Correlative control (influence of one organ over another organ) of seeds over maternal growth is one of the most obvious phenotypic expressions of the trade-off between growth and reproduction. However, the underlying molecular mechanisms are largely unknown. Here, we characterize the physiological and molecular effects of correlative inhibition by seeds on Arabidopsis (Arabidopsis thaliana) inflorescences, i.e. global proliferative arrest (GPA) during which all maternal growth ceases upon the production of a given number of seeds. We observed transcriptional responses to growth-and branching-inhibitory hormones, and low mitotic activity in meristems upon GPA, but found that meristems retain their identity and proliferative potential. In shoot tissues, we detected the induction of stress-and senescence-related gene expression upon fruit production and GPA, and a drop in chlorophyll levels, suggestive of altered source-sink relationships between vegetative shoot and reproductive tissues. Levels of shoot reactive oxygen species, however, strongly decreased upon GPA, a phenomenon that is associated with bud dormancy in some perennials. Indeed, gene expression changes in arrested apical inflorescences after fruit removal resembled changes observed in axillary buds following release from apical dominance. This suggests that GPA represents a form of bud dormancy, and that dominance is gradually transferred from growing inflorescences to maturing seeds, allowing offspring control over maternal resources, simultaneously restricting offspring number. This would provide a mechanistic explanation for the constraint between offspring quality and quantity.

show abstract

“…Between 12 and 190 million reads were analyzed per sample. Reads were aligned to the NCBI37/mm9 build of the Mus musculus genome using the Subread aligner (31). Genewise counts were obtained using featureCounts (32), and log2-reads per kilobase per million reads were averaged over replicates using voom (33).…”

Section: Irf4mentioning

confidence: 99%

Transcription Factor IRF4 Regulates Germinal Center Cell Formation through a B Cell–Intrinsic Mechanism

Willis

Good-Jacobson

Curtis

et al. 2014

The Journal of Immunology

Self Cite

107

View full text Add to dashboard Cite

In response to antigenic stimulation, mature B cells interact with follicular helper T cells in specialized structures called germinal centers (GCs), which leads to the development of memory B cells and Ab-secreting plasma cells. The transcription factor IFN regulatory factor 4 (IRF4) is essential for the formation of follicular helper T cells and thus GCs, although whether IRF4 plays a distinct role in GC B cells remains contentious. RNAseq analysis on ex vivo-derived mouse B cell populations showed that Irf4 was lowly expressed in naive B cells, highly expressed in plasma cells, but absent from GC B cells. In this study, we used conditional deletion of Irf4 in mature B cells as well as wild-type and Irf4-deficient mixed bone marrow chimeric mice to investigate how and where IRF4 plays its essential role in GC formation. Strikingly, GC formation was severely impaired in mice in which Irf4 was conditionally deleted in mature B cells, after immunization with protein Ags or infection with Leishmania major. This effect was evident as early as day 5 following immunization, before the development of GCs, indicating that Irf4 was required for the development of early GC B cells. This defect was B cell intrinsic because Irf4-deficient B cells in chimeric mice failed to participate in the GC in response to L. major or influenza virus infection. Taken together, these data demonstrate a B cell–intrinsic requirement for IRF4 for not only the development of Ab secreting plasma cells but also for GC formation.

show abstract

The Subread aligner: fast, accurate and scalable read mapping by seed-and-vote

Cited by 2,352 publications

References 50 publications

A point mutation in the Ncr1 signal peptide impairs the development of innate lymphoid cell subsets

A point mutation in the Ncr1 signal peptide impairs the development of innate lymphoid cell subsets

Seed Production Affects Maternal Growth and Senescence in Arabidopsis

Transcription Factor IRF4 Regulates Germinal Center Cell Formation through a B Cell–Intrinsic Mechanism

Contact Info

Product

Resources

About