Top 10 Biorxiv Papers Today in Genetics


2.053 Mikeys
#1. A large-scale multivariate pQTL study sheds light on the genetic architecture of obesity
Hélène Ruffieux, Jérôme Carayol, Mary Ellen Harper, Robert Dent, Wim Saris, Arne Astrup, Anthony Davison, Jorg Hager, Armand Valsesia
The genetic contribution to obesity has been widely studied, yet the functional mechanisms underlying metabolic states remain elusive. This has prompted analysis of endophenotypes via quantitative trait locus studies, which assess how genetic variants affect intermediate gene (eQTL) or protein (pQTL) expression phenotypes. To leverage shared regulatory patterns, we present the first integrative multivariate pQTL analysis, performed with our scalable Bayesian framework LOCUS on plasma mass-spectrometry and aptamer-based proteomic datasets. We identify 136 pQTL associations in the Ottawa obesity clinical practice, of which > 80% replicate in the DiOGenes obesity cohort and show significant functional enrichments; 16% of the validated hits would be missed by standard univariate methods. By also exploiting extensive clinical data, our methods and results reveal the implication of proteins under genetic control in low-grade inflammation, insulin resistance, and dyslipidemia, thereby opening new perspectives for diagnosing and treating...
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biorxivpreprint: A large-scale multivariate pQTL study sheds light on the genetic architecture of obesity https://t.co/97E8mUsQLB #bioRxiv
biorxiv_genetic: A large-scale multivariate pQTL study sheds light on the genetic architecture of obesity https://t.co/ndzgziRk9v #biorxiv_genetic
jessicabakerphd: RT @biorxiv_genetic: A large-scale multivariate pQTL study sheds light on the genetic architecture of obesity https://t.co/ndzgziRk9v #bio…
CamronBryantPhD: RT @biorxiv_genetic: A large-scale multivariate pQTL study sheds light on the genetic architecture of obesity https://t.co/ndzgziRk9v #bio…
gtimblin: RT @biorxivpreprint: A large-scale multivariate pQTL study sheds light on the genetic architecture of obesity https://t.co/97E8mUsQLB #bio…
Armand_v1: RT @biorxivpreprint: A large-scale multivariate pQTL study sheds light on the genetic architecture of obesity https://t.co/97E8mUsQLB #bio…
evogen_p: RT @biorxiv_genetic: A large-scale multivariate pQTL study sheds light on the genetic architecture of obesity https://t.co/ndzgziRk9v #bio…
Github

locus R package - Large-scale variational inference for combined covariate and response selection in sparse regression models

Repository: locus
User: hruffieux
Language: R
Stargazers: 4
Subscribers: 0
Forks: 1
Open Issues: 1
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Authors: 9
Total Words: 15487
Unqiue Words: 4086

2.024 Mikeys
#2. The landscape of SNCA transcripts across synucleinopathies: New insights from long reads sequencing analysis
Elizabeth Tseng, William J Rowell, Glenn Omolara-Chinue, Ting Hon, Julio Barrera, Steve Kujawa, Ornit Chiba-Falek
Dysregulation of alpha-synuclein expression has been implicated in the pathogenesis of synucleinopathies, in particular, Parkinson's Disease (PD) and Dementia with Lewy bodies (DLB). Previous studies have shown that the alternatively spliced isoforms of the SNCA gene are differentially expressed in different parts of the brain for PD and DLB patients. Similarly, SNCA isoforms with skipped exons can have a functional impact on the protein domains. The large intronic region of the SNCA gene was also shown to harbor structural variants that affect transcriptional levels. Here we apply the first study of using long read sequencing with targeted capture of both the gDNA and cDNA of the SNCA gene in brain tissues of PD, DLB, and control samples using the PacBio Sequel system. The targeted full-length cDNA (Iso-Seq) data confirmed complex usage of known alternative start sites and variable 3' UTR lengths, as well as novel 5' starts and 3' ends not previously described. The targeted gDNA data allowed phasing of up to 81% of the ~114kb...
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ScienceofPD: @PacBio & @Duke_Neurology researchers have an interesting manuscript on @biorxivpreprint outlining the first study of long read sequencing of #Parkinsons-associated alpha synclein, revealing long-range information not previously accessible https://t.co/yLUmEQztAI https://t.co/T8Jvhg90YC
Magdoll: Preprint on targeted gDNA + cDNA using @PacBio for SNCA gene on Parkinsons Disease! This is collaboration w/ Ornit Chiba-Falek (Duke) with analysis by me & @nothingclever! There's lots to discover with just 1 SMRT cell! https://t.co/YG1bmAajKD
AhmadAlKhleifat: The landscape of SNCA transcripts across synucleinopathies: New insights from long reads sequencing analysis | bioRxiv https://t.co/arWSXISlaP
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Sample Sizes : [12, 4, 4, 4]
Authors: 7
Total Words: 6230
Unqiue Words: 2127

2.02 Mikeys
#3. Improved polygenic prediction by Bayesian multiple regression on summary statistics
Luke R. Lloyd-Jones, Jian Zeng, Julia Sidorenko, Loic Yengo, Gerhard Moser, Kathryn E. Kemper, Huanwei Wang, Zhili Zheng, Reedik Magi, Tonu Esko, Andres Metspalu, Naomi R. Wray, Michael E. Goddard, Jian Yang, Peter M. Visscher
The capacity to accurately predict an individual's phenotype from their DNA sequence is one of the great promises of genomics and precision medicine. Recently, Bayesian methods for generating polygenic predictors have been successfully applied in human genomics but require the individual level data, which are often limited in their access due to privacy or logistical concerns, and are computationally very intensive. This has motivated methodological frameworks that utilise publicly available genome-wide association studies (GWAS) summary data, which now for some traits include results from greater than a million individuals. In this study, we extend the established summary statistics methodological framework to include a class of point-normal mixture prior Bayesian regression models, which have been shown to generate optimal genetic predictions and can perform heritability estimation, variant mapping and estimate the distribution of the genetic effects. In a wide range of simulations and cross-validation using 10 real quantitative...
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biorxivpreprint: Improved polygenic prediction by Bayesian multiple regression on summary statistics https://t.co/cQ0KBuLSmV #bioRxiv
razibkhan: Improved polygenic prediction by Bayesian multiple regression on summary statistics https://t.co/ApW3drlOVJ #genetics
GWAS_lit: Improved polygenic prediction by Bayesian multiple regression on summary statistics https://t.co/wAymXjFj9J https://t.co/5ny9Dsr5Gq
biorxiv_genetic: Improved polygenic prediction by Bayesian multiple regression on summary statistics https://t.co/C1XxjXW1rP #biorxiv_genetic
arjunmanrai: Improved polygenic prediction by Bayesian multiple regression on summary statistics | bioRxiv https://t.co/q2MejKcGoH
LalDennis: ! Improved polygenic prediction by Bayesian multiple regression on summary statistics https://t.co/dEDboqLAEQ https://t.co/z8YhCdszEd
PCTGenomics: Our paper outlining a new summary-based method for polygenic prediction is now on bioRxiv https://t.co/D5wLQlFXo0 @IMBatUQ @UQ_News
Robertlloydjone: Improved polygenic prediction by Bayesian multiple regression on summary statistics https://t.co/5cEPQlMUV3
EquusAnalytics: Improved polygenic prediction by Bayesian multiple regression on summary statistics https://t.co/0vDaxkThSM
skathire: RT @biorxiv_genetic: Improved polygenic prediction by Bayesian multiple regression on summary statistics https://t.co/C1XxjXW1rP #biorxiv_…
casey6r0wn: RT @biorxiv_genetic: Improved polygenic prediction by Bayesian multiple regression on summary statistics https://t.co/C1XxjXW1rP #biorxiv_…
dccc_phd: RT @arjunmanrai: Improved polygenic prediction by Bayesian multiple regression on summary statistics | bioRxiv https://t.co/q2MejKcGoH
jyang1981: RT @biorxiv_genetic: Improved polygenic prediction by Bayesian multiple regression on summary statistics https://t.co/C1XxjXW1rP #biorxiv_…
LS_Hall: RT @biorxiv_genetic: Improved polygenic prediction by Bayesian multiple regression on summary statistics https://t.co/C1XxjXW1rP #biorxiv_…
AGDAYWILL: RT @GWAS_lit: Improved polygenic prediction by Bayesian multiple regression on summary statistics https://t.co/wAymXjFj9J https://t.co/5ny9…
Q_StatGen: RT @biorxiv_genetic: Improved polygenic prediction by Bayesian multiple regression on summary statistics https://t.co/C1XxjXW1rP #biorxiv_…
m_foll: RT @biorxiv_genetic: Improved polygenic prediction by Bayesian multiple regression on summary statistics https://t.co/C1XxjXW1rP #biorxiv_…
robbeewedow: RT @GWAS_lit: Improved polygenic prediction by Bayesian multiple regression on summary statistics https://t.co/wAymXjFj9J https://t.co/5ny9…
Martin_Tobin: RT @GWAS_lit: Improved polygenic prediction by Bayesian multiple regression on summary statistics https://t.co/wAymXjFj9J https://t.co/5ny9…
dajiangliu81: RT @GWAS_lit: Improved polygenic prediction by Bayesian multiple regression on summary statistics https://t.co/wAymXjFj9J https://t.co/5ny9…
socalsysbio: RT @biorxiv_genetic: Improved polygenic prediction by Bayesian multiple regression on summary statistics https://t.co/C1XxjXW1rP #biorxiv_…
MiguelSieck: RT @biorxiv_genetic: Improved polygenic prediction by Bayesian multiple regression on summary statistics https://t.co/C1XxjXW1rP #biorxiv_…
akousathanas: RT @GWAS_lit: Improved polygenic prediction by Bayesian multiple regression on summary statistics https://t.co/wAymXjFj9J https://t.co/5ny9…
Inga_genetics: RT @GWAS_lit: Improved polygenic prediction by Bayesian multiple regression on summary statistics https://t.co/wAymXjFj9J https://t.co/5ny9…
LorettoM: RT @biorxiv_genetic: Improved polygenic prediction by Bayesian multiple regression on summary statistics https://t.co/C1XxjXW1rP #biorxiv_…
vanessa_higham: RT @GWAS_lit: Improved polygenic prediction by Bayesian multiple regression on summary statistics https://t.co/wAymXjFj9J https://t.co/5ny9…
ReechaSofat: RT @biorxiv_genetic: Improved polygenic prediction by Bayesian multiple regression on summary statistics https://t.co/C1XxjXW1rP #biorxiv_…
genomegenie: RT @PCTGenomics: Our paper outlining a new summary-based method for polygenic prediction is now on bioRxiv https://t.co/D5wLQlFXo0 @IMBa…
zjuwhw: RT @PCTGenomics: Our paper outlining a new summary-based method for polygenic prediction is now on bioRxiv https://t.co/D5wLQlFXo0 @IMBa…
sharmavarun840: RT @razibkhan: Improved polygenic prediction by Bayesian multiple regression on summary statistics https://t.co/ApW3drlOVJ #genetics
jakob_grove: RT @biorxiv_genetic: Improved polygenic prediction by Bayesian multiple regression on summary statistics https://t.co/C1XxjXW1rP #biorxiv_…
zhaowenliu_kaka: RT @GWAS_lit: Improved polygenic prediction by Bayesian multiple regression on summary statistics https://t.co/wAymXjFj9J https://t.co/5ny9…
evogen_p: RT @biorxiv_genetic: Improved polygenic prediction by Bayesian multiple regression on summary statistics https://t.co/C1XxjXW1rP #biorxiv_…
DiegoV_O_: RT @GWAS_lit: Improved polygenic prediction by Bayesian multiple regression on summary statistics https://t.co/wAymXjFj9J https://t.co/5ny9…
margaretlippin2: RT @biorxiv_genetic: Improved polygenic prediction by Bayesian multiple regression on summary statistics https://t.co/C1XxjXW1rP #biorxiv_…
YingJi_Vandy: RT @GWAS_lit: Improved polygenic prediction by Bayesian multiple regression on summary statistics https://t.co/wAymXjFj9J https://t.co/5ny9…
Nuno11878867: RT @GWAS_lit: Improved polygenic prediction by Bayesian multiple regression on summary statistics https://t.co/wAymXjFj9J https://t.co/5ny9…
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Sample Sizes : [347106, 341819, 197789, 317502, 346738, 341633, 317502, 347231, 347198, 197778, 346738, 197789]
Authors: 15
Total Words: 16336
Unqiue Words: 3847

2.019 Mikeys
#4. Deep phenotyping of a healthy human HAO1 knockout informs therapeutic development for primary hyperoxaluria type 1.
Tracy L McGregor, Karen A Hunt, Paul Nioi, Dan Mason, Simina Ticau, Marissa Pelosi, Loken Perry, Sarah Finer, Christopher Griffiths, Daniel MacArthur, Richard C Trembath, Devin Oglesbee, John Lieske, John Wright, David Erbe, David van Heel
Primary Hyperoxaluria Type 1 (PH1) is a rare autosomal recessive metabolic disorder of oxalate metabolism leading to kidney failure as well as multi-organ damage. Overproduction of oxalate occurs in the liver due to an inherited genetic defect in the enzyme alanine-glyoxylate aminotransferase ( AGXT ), causing pathology due to the insolubility of calcium oxalate crystals in body fluids. The main current therapy is dual liver-kidney transplant, which incurs high morbidity and has poor availability in some health systems where PH1 is more prevalent. One approach currently in active clinical investigation targets HAO1 (hydroxyacid oxidase 1), encoding glycolate oxidase, to reduce substrate levels for oxalate production. To inform drug development, we sought individuals with reduced HAO1 function due to naturally occurring genetic variation. Analysis of loss of function variants in 141,456 sequenced individuals suggested individuals with complete HAO1 knockout would only be observed in 1 in 30 million outbred people. However in a...
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stuartacook1: Super, super nice study. I would love to do this with the human IL11RA1 KOs who are out there. https://t.co/SGLBGZK2m1
jthteo: WOW. Impressive methodology for the future of precision medicine. Genetics and EHR deep phenotyping to identify presymptomatic rare disease..... https://t.co/UskAriraQe
fanuel_z: Deep phenotyping of a healthy human HAO1 knockout informs therapeutic development for primary hyperoxaluria type 1. https://t.co/jzcoa9Ubo1
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Sample Sizes : [67, 67]
Authors: 16
Total Words: 5181
Unqiue Words: 1889

2.007 Mikeys
#5. S. cerevisiae Srs2 helicase ensures normal recombination intermediate metabolism during meiosis and prevents accumulation of Rad51 aggregates
Laura J Hunt, Emad Ahmed, Hardeep Kaur, Jasvinder Ahuja, Lydia Hulme, Ta-Chung Chou, Michael Lichten, Alastair S.H. Goldman
We investigated the meiotic role of Srs2, a multi-functional DNA helicase/translocase that destabilizes Rad51-DNA filaments, and is thought to regulate strand invasion and prevent hyper-recombination during the mitotic cell cycle. We find that Srs2 activity is required for normal meiotic progression and spore viability. A significant fraction of srs2 mutant cells progress through both meiotic divisions without separating the bulk of their chromatin, although sister centromeres often separate. Undivided nuclei contain aggregates of Rad51 colocalized with the ssDNA-binding protein RPA, suggesting the presence of persistent single-strand DNA. Rad51 aggregate formation requires Spo11-induced DSBs, Rad51 strand-invasion activity, and progression past the pachytene stage of meiosis, but not the DSB end-resection or the bias towards inter-homologue strand invasion characteristic of normal meiosis. srs2 mutants also display altered meiotic recombination intermediate metabolism, revealed by defects in the formation of stable joint...
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DoctorAnneG: A new article from our Dean on better understanding of meiosis mechanisms in yeast https://t.co/v79s4rXOIX
DrLJHunt: Very, very excited that my thesis work has made its way to the real world! Well.. the preprint world at least ;) Also very, very grateful to the Lichten & Shinohara labs! https://t.co/eu8yGj2UOA
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Sample Sizes : None.
Authors: 8
Total Words: 11200
Unqiue Words: 3174

2.004 Mikeys
#6. LipoGlo: A sensitive and specific reporter of atherogenic lipoproteins
James H Thierer, Steven Farber, Stephen Ekker
Apolipoprotein-B (APOB) is the structural component of atherogenic lipoproteins, lipid-rich particles that drive atherosclerosis by accumulating in the vascular wall. As atherosclerotic cardiovascular disease is the leading cause of death worldwide, there is an urgent need to develop new strategies to prevent lipoproteins from causing vascular damage. Here we report the LipoGlo system, which uses a luciferase enzyme (NanoLuc) fused to ApoB to monitor several key determinants of lipoprotein atherogenicity including particle abundance, size, and localization. Using LipoGlo, we are able to comprehensively characterize the lipoprotein profile of individual larval zebrafish and collect the first images of atherogenic lipoprotein localization in an intact organism. We discover multiple unexpected extravascular lipoprotein localization patterns, as well as identify pla2g12b as a potent regulator of lipoprotein size. ApoB-fusion proteins thus represent a uniquely sensitive and specific approach to study atherogenic lipoproteins and their...
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stefarber: LipoGlo: A sensitive and specific reporter of atherogenic lipoproteins https://t.co/zm1fWqUMc7
CarnegieDevBio: RT @stefarber: LipoGlo: A sensitive and specific reporter of atherogenic lipoproteins https://t.co/zm1fWqUMc7
ZebrafishRock: RT @stefarber: LipoGlo: A sensitive and specific reporter of atherogenic lipoproteins https://t.co/zm1fWqUMc7
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Sample Sizes : [24, 30, 30, 9, 9, 9, 9, 9, 15, 15, 15, 15, 15, 15, 15, 4, 9]
Authors: 3
Total Words: 18983
Unqiue Words: 5491

2.002 Mikeys
#7. Investigating causal pathways between liability to ADHD and substance use, and liability to substance use and ADHD risk, using Mendelian randomization.
Jorien Treur, Ditte Demontis, Hannah Sallis, ADHD working group of the Psychiatric Genomics Consortium, Thomas Richardson, Reinout Wiers, Anders Borglum, Karin Verweij, Marcus Munafo
Background: Attention-deficit hyperactivity disorder (ADHD) has consistently been associated with substance (ab)use, but the nature of this association is not fully understood. In view of preventive efforts, a vital question is whether there are causal effects, from ADHD to substance use and/or from substance use to ADHD. Methods: We applied bidirectional Mendelian randomization using summary-level data from the largest available genome-wide association studies (GWASs) on ADHD, smoking (initiation, cigarettes per day, cessation, and a compound measure of lifetime smoking), alcohol use (drinks/week and alcohol use disorder), cannabis use (initiation and cannabis use disorder (CUD)) and coffee consumption (cups/day). Genetic variants robustly associated with the exposure were selected as instruments and then identified in the outcome GWAS. Effect estimates from individual genetic variants were combined with inverse-variance weighted regression and five sensitivity analyses were applied (weighted median, weighted mode, MR-Egger,...
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RenatoPolimanti: Investigating causal pathways between liability to ADHD and substance use, and liability to substance use and ADHD risk, using Mendelian randomization #bioRxiv #ADHD #smoking #drinking #cannabis #GWAS #Mendelian #Randomization @MarcusMunafo @PGCgenetics https://t.co/jAjf5bD1oc
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Sample Sizes : [144, 55374, 1232091, 263952, 312817, 463003, 941280, 121630, 162082, 51372, 91462, 632783, 15548]
Authors: 9
Total Words: 8352
Unqiue Words: 2263

1.999 Mikeys
#8. Targeted Long-Read RNA Sequencing Demonstrates Transcriptional Diversity Driven by Splice-Site Variation in MYBPC3
Alexandra Dainis, Elizabeth Tseng, Tyson A Clark, Ting Hon, Matthew Wheeler, Euan Ashley
Background: Clinical sequencing has traditionally focused on genomic DNA through the use of targeted panels and exome sequencing, rather than investigating the potential transcriptomic consequences of disease-associated variants. RNA sequencing has recently been shown to be an effective additional tool for identifying disease-causing variants. We here use targeted long-read genome and transcriptome sequencing to efficiently and economically identify molecular consequences of a rare, disease-associated variant in hypertrophic cardiomyopathy (HCM). Methods and Results: Our study, which employed both Pacific Biosciences SMRT sequencing and Oxford Nanopore Technologies MinION sequencing, as well as two RNA targeting strategies, identified alternatively-spliced isoforms that resulted from a splice-site variant containing allele in HCM. These included a predicted in-frame exon-skipping event, as well as an abundance of additional isoforms with unexpected intron-inclusion, exon-extension, and pseudo-exon events. The use of long-read RNA...
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_adameur: Nice approach using long reads to study RNA consequences of a disease causing splice variant https://t.co/PSw3EZsWRD
jsantoyo: Targeted Long-Read RNA Sequencing Demonstrates Transcriptional Diversity Driven by Splice-Site Variation in MYBPC3. https://t.co/ymVySGHQ2n
tingfordha: RT @_adameur: Nice approach using long reads to study RNA consequences of a disease causing splice variant https://t.co/PSw3EZsWRD
TJesse62: RT @_adameur: Nice approach using long reads to study RNA consequences of a disease causing splice variant https://t.co/PSw3EZsWRD
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Sample Sizes : None.
Authors: 6
Total Words: 7988
Unqiue Words: 2095

1.998 Mikeys
#9. Scarless Enriched selection of Genome edited Human Pluripotent Stem Cells Using Induced Drug Resistance
Keun-Tae Kim, Ju-Chan Park, Haesung Lee, Hyeon-Ki Jang, Yang Jin, Wankyu Kim, Jeongmi Lee, Hyongbum Henry Kim, Sangsu Bae, Hyuk-Jin Cha
An efficient gene editing technique for use in human pluripotent stem cells (hPSCs) would have great potential value in regenerative medicine, as well as in drug discovery based on isogenic human disease models. However, the extremely low efficiency of gene editing in hPSCs is a major technical hurdle that remains to be resolved. Previously, we demonstrated that YM155, a survivin inhibitor developed as an anti-cancer drug, induces highly selective cell death in undifferentiated hPSCs. In this study, we demonstrated that the high cytotoxicity of YM155 in hPSCs, which is mediated by selective cellular uptake of the drug, is due to high expression of SLC35F2 in these cells. Consistent with this, knockout of SLC35F2 with CRISPR-Cas9 or depletion with siRNAs made hPSCs highly resistant to YM155. Simultaneous gene editing of a gene of interest and transient knockdown of SLC35F2 following YM155 treatment enabled genome-edited hPSCs to survive because YM155 resistance was temporarily induced, thereby achieving enriched selection of...
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biorxivpreprint: Scarless Enriched selection of Genome edited Human Pluripotent Stem Cells Using Induced Drug Resistance https://t.co/Hi8inZU45U #bioRxiv
UoM_TgU: Scarless Enriched selection of Genome edited Human Pluripotent Stem Cells Using Induced Drug Resistance https://t.co/f5NRnJJTA4
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Sample Sizes : None.
Authors: 10
Total Words: 8942
Unqiue Words: 2555

1.997 Mikeys
#10. Synaptonemal complex proteins direct and constrain the localization of crossover-promoting proteins during Caenorhabditis elegans meiosis
Diana E Libuda, Cori K Cahoon, Jacquellyn M Helm
Crossovers (COs) between homologous chromosomes are critical for meiotic chromosome segregation and form in the context of the synaptonemal complex (SC), a meiosis-specific structure that assembles between aligned homologs. During Caenorhabditis elegans meiosis, central region components of the SC (SYP proteins) are essential to repair double-strand DNA breaks (DSBs) as COs, but the roles of these SYP proteins in promoting CO formation are poorly understood. Here, we investigate the relationships between the SYP proteins and conserved CO-promoting factors by examining the immunolocalization of these factors in meiotic mutants where SYP proteins are absent, reduced, or mis-localized. Although COs do not form in syp null mutants, CO-promoting proteins COSA-1, MSH-5, and ZHP-3 nevertheless become co-localized at a variable number of DSB-dependent sites during late prophase, reflecting an inherent affinity of these factors for DSB repair sites. In contrast, in mutants where SYP proteins are present but form aggregates or display...
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lichtenmj: Synaptonemal complex proteins direct and constrain the localization of crossover-promoting proteins during Caenorhabditis elegans meiosis https://t.co/UznGEzAyy2
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Sample Sizes : [505, 223, 101, 99, 505, 161, 28, 40, 505, 245, 213, 193, 226, 162, 103, 100]
Authors: 3
Total Words: 10242
Unqiue Words: 2162

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