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Articles by Jonathan Flint
Cell-type-specific eQTLs underlie the genetic architecture of complex traits
Abstract Genetic effects on complex traits primarily act by regulating gene expression; however, this process is not well understood1. Studies of genetic effects on gene expression (expression quantitative trait loci (eQTLs)) can inform as to the gene regulatory layer between genetic variants and complex traits2. However, previous studies have not effectively captured cell-type-specific eQTLs, which are likely to be important for complex traits.
Silkworms, by Long Ling, Translated by Jonathan Flint
The restaurant is still there. Cars line both sides of the street, so I have to park a block away. I am carrying a five-foot pole and a pair of scissors in a plastic bag.
The relationship between genotype- and phenotype-based estimates of genetic liability to psychiatric disorders, in practice and in theory
Keywords genetics family genetic risk scores genetic liability polygenic risk scores psychiatric disorders Get full text access Log in, subscribe or purchase for full access. References 1. Falconer, D.S. Introduction to Quantitative Genetics Prentice Hall, Harlow, 1996 2. Lynch, M. & Walsh, B. (1998) Genetics and Analysis of Quantitative Traits. (Sinauer). 3. Goddard, M.E. ∙ Hayes, B.J. Genomic selection J. Anim. Breed. Genet. 2007; 124:323-330 4. Meuwissen, T. ∙ Hayes, B. ∙ Goddard, M.
Jonathan Flint | A Diagnosis
The day before James Watson arrived to deliver the 2013 Michael Davys Lecture in Oxford, I received an email from his personal physician in New York asking me to arrange for him to be seen by ‘one of your best surgeons’ to remove a skin tumour. Since I had invited Watson to Oxford, it seemed I was also now responsible for his medical treatment. Fearing catastrophe, I asked Peter Ratcliffe for advice. ‘What we need is a diagnosis,’ he said, and recommended four dermatologists.
Jonathan Flint and Iain Mathieson
Most women who undertake IVF will have their embryos screened for genetic abnormalities. Clinics in some parts of the world also offer to select an embryo for implantation based on genetic markers for everything from eye and hair colour to behavioural, emotional and cognitive traits. The next, far more consequential, step is the genome editing of human embryos.
Deep learning-based phenotype imputation on population-scale biobank data increases genetic discoveries - Nature Genetics
Abstract Biobanks that collect deep phenotypic and genomic data across many individuals have emerged as a key resource in human genetics. However, phenotypes in biobanks are often missing across many individuals, limiting their utility. We propose AutoComplete, a deep learning-based imputation method to impute or ‘fill-in’ missing phenotypes in population-scale biobank datasets.
Phenotype integration improves power and preserves specificity in biobank-based genetic studies of major depressive disorder - Nature Genetics
Abstract Biobanks often contain several phenotypes relevant to diseases such as major depressive disorder (MDD), with partly distinct genetic architectures. Researchers face complex tradeoffs between shallow (large sample size, low specificity/sensitivity) and deep (small sample size, high specificity/sensitivity) phenotypes, and the optimal choices are often unclear. Here we propose to integrate these phenotypes to combine the benefits of each.
Author Correction: Sparse whole-genome sequencing identifies two loci for major depressive disorder - Nature
Correction to: Nature https://doi.org/10.1038/nature14659 Published online 15 July 2015 We are updating the section on data availability for this article. The genotype and whole genome sequence data used in this publication were made publicly available at the time of publication through the GigaDB database at http://gigadb.org/dataset/100155. The whole genome sequence data files were subsequently withdrawn from GigaDB following a change in data sharing regulations in China.
The genetic basis of major depressive disorder - Molecular Psychiatry
It’s sometimes claimed that MDD cases identified by minimal phenotyping are just less severe forms of MDD, and thus share the same genetic loci [1]. That would be equivalent to lowering the threshold for disease liability in the population above which “cases” for MDD are defined.
Phenotypic subtyping via contrastive learning
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Behavioral genetics in the 21st century
The field of behavioral genetics has always attracted controversy and nowhere more so than when it addresses the genetic basis of intelligence. Not only has the existence of such genetic effects been vigorously denied, but those who claim to have identified them have been accused of being eugenicists or worse. Leon Kamin’s The Science and Politics of I.Q. 1 Kamin L.J. The Science and Politics of I.Q..
Jonathan Flint · Testing Woes · LRB 6 May 2021
Ayear ago I joined half a dozen academics at the University of California in Los Angeles, a group of physicians, geneticists and computational biologists, to try to help address the public health challenge of asymptomatic Covid-19 transmission.
Genesis of a complex disease
The largest genome-wide analysis of schizophrenia performed so far has identified more than 100 genetic regions that contribute to disease risk, establishing new leads for understanding this form of mental illness. See Article p.421 A paper1 published this week in Nature marks the culmination of a long debate about the genetic basis of a disorder sometimes considered psychiatry's heartland2 — schizophrenia. No other psychiatric condition has evoked such diverse opinions.
The great hairball gambit
Loading metrics Open Access Opinion Piece Jonathan Flint , Trey Ideker Jonathan Flint, Trey Ideker Published: November 26, 2019 https://doi.org/10.1371/journal.pgen.1008519 ? This is an uncorrected proof. Citation: Flint J, Ideker T (2019) The great hairball gambit. PLoS Genet 15(11): e1008519. https://doi.org/10.1371/journal.pgen.1008519 Editor: Gregory P. Copenhaver, The University of North Carolina at Chapel Hill, UNITED STATES Published: November 26, 2019 Copyright: © 2019 Flint, Ideker.
Outside in
Citation: Flint J (2019) Outside in. PLoS Genet 15(2): e1008014. https://doi.org/10.1371/journal.pgen.1008014 Published: February 28, 2019 Copyright: © 2019 Jonathan Flint. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Funding: The author received no specific funding for this work.
GxEMM: Extending linear mixed models to general gene-environment interactions
GxEMM: Extending linear mixed models to general gene-environment interactions Andy Dahl, Na Cai, Jonathan Flint, Noah Zaitlen bioRxiv 397638; doi: https://doi.org/10.1101/397638
Deep Reads: How I learnt to love population genetics
I’m not sure when I bought my copy of James F. Crow’s “Basic Concepts in Population, Quantitative and Evolutionary Genetics” [1] but it could not have been too long after the first edition came out in 1986 (there is a stub of a plane ticket in my copy dated 1994, so I must have bought it before then; for a good many years around that time the book was a comfort item for me; Fig 1).
The meaning of life
I don’t think I’ve talked much about the meaning of life since I was a teenager, but recently I did just that with some friends over dinner in Los Angeles. Naturally, as a geneticist, I could confidently assure everyone around the table that evening that life has no meaning. Life’s only purpose is to ensure the transmission of DNA from one generation to the next. What I forgot to add in the ensuing uproar (“well your life may have no meaning, but mine certainly does”) was the question: whose DNA?
Deep Reads: How I learnt to love population genetics
I’m not sure when I bought my copy of James F. Crow’s “Basic Concepts in Population, Quantitative and Evolutionary Genetics” [1] but it could not have been too long after the first edition came out in 1986 (there is a stub of a plane ticket in my copy dated 1994, so I must have bought it before then; for a good many years around that time the book was a comfort item for me; Fig 1).
Gunman shoots 3 at apartment complex before killing self | My FOX Spokane
CHEYENNE, Wyo. (AP) – A gunman shot three people – killing one – at a senior citizen apartment complex in Cheyenne on Wednesday morning before killing himself as officers closed in on him, police said. One of the three people shot by the gunman is dead, said Dan Long, spokesman for the Cheyenne Police Department. There’s no immediate word on the condition of the other two victims.
Tough Phoenix sheriff may have new foe: George Soros | My FOX Spokane
PHOENIX (AP) – Joe Arpaio, the self-proclaimed toughest sheriff in America who could face criminal charges for ignoring a judge’s order to stop targeting Latinos in anti-immigration roundups, may now have a new foe as he seeks re-election – George Soros, the billionaire liberal hedge fund tycoon.
Man charged in North Carolina cop’s slaying to be arraigned | My FOX Spokane
COVENTRY, R.I. (AP) – A wounded fugitive wanted in connection with the fatal shooting of a police officer in North Carolina was scheduled to be arraigned Wednesday evening, hours after he was captured by police in Rhode Island, state police said. Fenner was taken to a hospital for treatment of a gunshot wound. State Police Col. Steven O’Donnell said Fenner was wounded during the shootout Saturday with 38-year-old Shelby police Officer Tim Brackeen in the North Carolina city. Brackeen died Monday.
G = E: What GWAS Can Tell Us about the Environment
Citation: Gage SH, Davey Smith G, Ware JJ, Flint J, Munafò MR (2016) G = E: What GWAS Can Tell Us about the Environment. PLoS Genet12(2): e1005765. https://doi.org/10.1371/journal.pgen.1005765 Copyright: © 2016 Gage et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Schizophrenia: Genesis of a complex disease
A paper1 published this week in Nature marks the culmination of a long debate about the genetic basis of a disorder sometimes considered psychiatry's heartland2 — schizophrenia. No other psychiatric condition has evoked such diverse opinions. Its biological roots have often been denied and, in the anti-psychiatry movement of the 1970s, there was even outright rejection of its existence.
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