From 403b6bd7d6bc7d4d40cf4e76b35cc1adc01f63a6 Mon Sep 17 00:00:00 2001 From: "Abolfazl (Abe)" Date: Sat, 6 Apr 2024 05:35:57 -0700 Subject: [PATCH] update references related to #7 --- docs/source/references.bib | 11 ----------- docs/source/references.rst | 4 +++- 2 files changed, 3 insertions(+), 12 deletions(-) diff --git a/docs/source/references.bib b/docs/source/references.bib index a73212b..8fd1972 100644 --- a/docs/source/references.bib +++ b/docs/source/references.bib @@ -6,14 +6,11 @@ @article {Herken2023 doi = {10.1101/2023.08.09.552346}, publisher = {Cold Spring Harbor Laboratory}, abstract = {A fundamental question in biology is how a limited number of genes combinatorially govern cellular responses to environmental changes. While the prevailing hypothesis is that relationships between genes, processes, and ontologies could be plastic to achieve this adaptability, quantitatively comparing human gene functional connections between specific environmental conditions at scale is very challenging. Therefore, it remains unclear whether and how human genetic interaction networks are rewired in response to changing environmental conditions. Here, we developed a framework for mapping context-specific genetic interactions, enabling us to measure the plasticity of human genetic architecture upon environmental challenge for \~{}250,000 interactions, using cell cycle interruption, genotoxic perturbation, and nutrient deprivation as archetypes. We discover large-scale rewiring of human gene relationships across conditions, highlighted by dramatic shifts in the functional connections of epigenetic regulators (TIP60), cell cycle regulators (PP2A), and glycolysis metabolism. Our study demonstrates that upon environmental perturbation, intra-complex genetic rewiring is rare while inter-complex rewiring is common, suggesting a modular and flexible evolutionary genetic strategy that allows a limited number of human genes to enable adaptation to a large number of environmental conditions.One Sentence Summary Five human genetic interaction maps reveal how the landscape of genes{\textquoteright} functional relationships is rewired as cells experience environmental stress to DNA integrity, cell cycle regulation, and metabolism.Competing Interest StatementL.A.G and T.M.N. have filed patents on CRISPR functional genomics. L.A.G consults for, has equity in and is a co-founder of Chroma Medicine.}, - URL = {https://www.biorxiv.org/content/early/2023/08/09/2023.08.09.552346}, - eprint = {https://www.biorxiv.org/content/early/2023/08/09/2023.08.09.552346.full.pdf}, journal = {bioRxiv} } @article{Hsiung2023, title = {Higher-order combinatorial chromatin perturbations by engineered CRISPR-Cas12a for functional genomics}, - url = {http://dx.doi.org/10.1101/2023.09.18.558350}, DOI = {10.1101/2023.09.18.558350}, publisher = {Cold Spring Harbor Laboratory}, author = {Hsiung, CC and Wilson, CM and Sambold, NA and Dai, R and Chen, Q and Misiukiewicz, S and Arab, A and Teyssier, N and O’Loughlin, T and Cofsky, JC and Shi, J and Gilbert, LA}, @@ -25,7 +22,6 @@ @article{Han2020 title = {CRISPR screens in cancer spheroids identify 3D growth-specific vulnerabilities}, volume = {580}, ISSN = {1476-4687}, - url = {http://dx.doi.org/10.1038/s41586-020-2099-x}, DOI = {10.1038/s41586-020-2099-x}, number = {7801}, journal = {Nature}, @@ -40,7 +36,6 @@ @article{Han2017 title = {Synergistic drug combinations for cancer identified in a CRISPR screen for pairwise genetic interactions}, volume = {35}, ISSN = {1546-1696}, - url = {http://dx.doi.org/10.1038/nbt.3834}, DOI = {10.1038/nbt.3834}, number = {5}, journal = {Nature Biotechnology}, @@ -55,7 +50,6 @@ @article{Tian2019 title = {CRISPR Interference-Based Platform for Multimodal Genetic Screens in Human iPSC-Derived Neurons}, volume = {104}, ISSN = {0896-6273}, - url = {http://dx.doi.org/10.1016/j.neuron.2019.07.014}, DOI = {10.1016/j.neuron.2019.07.014}, number = {2}, journal = {Neuron}, @@ -70,7 +64,6 @@ @article{Horlbeck2016 title = {Compact and highly active next-generation libraries for CRISPR-mediated gene repression and activation}, volume = {5}, ISSN = {2050-084X}, - url = {http://dx.doi.org/10.7554/eLife.19760}, DOI = {10.7554/elife.19760}, journal = {eLife}, publisher = {eLife Sciences Publications, Ltd}, @@ -83,7 +76,6 @@ @article{Gilbert2014 title = {Genome-Scale CRISPR-Mediated Control of Gene Repression and Activation}, volume = {159}, ISSN = {0092-8674}, - url = {http://dx.doi.org/10.1016/j.cell.2014.09.029}, DOI = {10.1016/j.cell.2014.09.029}, number = {3}, journal = {Cell}, @@ -98,7 +90,6 @@ @article{Kampmann2014 title = {Functional genomics platform for pooled screening and generation of mammalian genetic interaction maps}, volume = {9}, ISSN = {1750-2799}, - url = {http://dx.doi.org/10.1038/nprot.2014.103}, DOI = {10.1038/nprot.2014.103}, number = {8}, journal = {Nature Protocols}, @@ -113,7 +104,6 @@ @article{Kampmann2013 title = {Integrated platform for genome-wide screening and construction of high-density genetic interaction maps in mammalian cells}, volume = {110}, ISSN = {1091-6490}, - url = {http://dx.doi.org/10.1073/pnas.1307002110}, DOI = {10.1073/pnas.1307002110}, number = {25}, journal = {Proceedings of the National Academy of Sciences}, @@ -127,7 +117,6 @@ @article{Bassik2013 title = {A Systematic Mammalian Genetic Interaction Map Reveals Pathways Underlying Ricin Susceptibility}, volume = {152}, ISSN = {0092-8674}, - url = {http://dx.doi.org/10.1016/j.cell.2013.01.030}, DOI = {10.1016/j.cell.2013.01.030}, number = {4}, journal = {Cell}, diff --git a/docs/source/references.rst b/docs/source/references.rst index 21b378c..14fc766 100644 --- a/docs/source/references.rst +++ b/docs/source/references.rst @@ -2,6 +2,8 @@ References ---------- * :cite:t:`Herken2023` *bioRxiv* - Gilbert Lab +* :cite:t:`Hsiung2023` *bioRxiv* - Gilbert Lab + * :cite:t:`Han2020` *Nature* - Bassik Lab * :cite:t:`Han2017` *Nature Biotechnology* - Bassik Lab @@ -22,4 +24,4 @@ References ============= .. bibliography:: - :cited: + :all: