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Article ; Online: Context-specific functions of chromatin remodellers in development and disease.

Gourisankar, Sai / Krokhotin, Andrey / Wenderski, Wendy / Crabtree, Gerald R

2023 Volume 25, Issue 5, Page(s) 340–361

Abstract: Chromatin remodellers were once thought to be highly redundant and nonspecific in their actions. However, recent human genetic studies demonstrate remarkable biological specificity and dosage sensitivity of the thirty-two adenosine triphosphate (ATP)- ... ...

Abstract	Chromatin remodellers were once thought to be highly redundant and nonspecific in their actions. However, recent human genetic studies demonstrate remarkable biological specificity and dosage sensitivity of the thirty-two adenosine triphosphate (ATP)-dependent chromatin remodellers encoded in the human genome. Mutations in remodellers produce many human developmental disorders and cancers, motivating efforts to investigate their distinct functions in biologically relevant settings. Exquisitely specific biological functions seem to be an emergent property in mammals, and in many cases are based on the combinatorial assembly of subunits and the generation of stable, composite surfaces. Critical interactions between remodelling complex subunits, the nucleosome and other transcriptional regulators are now being defined from structural and biochemical studies. In addition, in vivo analyses of remodellers at relevant genetic loci have provided minute-by-minute insights into their dynamics. These studies are proposing new models for the determinants of remodeller localization and function on chromatin.
MeSH term(s)	Animals ; Humans ; Chromatin/genetics ; Transcription Factors/genetics ; Chromatin Assembly and Disassembly ; Nucleosomes/genetics ; Genome, Human ; Mammals/genetics
Chemical Substances	Chromatin ; Transcription Factors ; Nucleosomes
Language	English
Publishing date	2023-11-24
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2035157-4
ISSN	1471-0064 ; 1471-0056
ISSN (online)	1471-0064
ISSN	1471-0056
DOI	10.1038/s41576-023-00666-x
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Zs.MG 40: Show issues

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Article: Rethinking our intellectual origins: response to Kalinka et al.

Crabtree, Gerald R

Trends in genetics : TIG

2013 Volume 29, Issue 3, Page(s) 127–129

MeSH term(s)	Evolution, Molecular ; Genomic Instability/physiology ; Humans ; Intelligence/genetics
Language	English
Publishing date	2013-03
Publishing country	England
Document type	Comment ; Letter
ZDB-ID	619240-3
ISSN	1362-4555 ; 0168-9525 ; 0168-9479
ISSN (online)	1362-4555
ISSN	0168-9525 ; 0168-9479
DOI	10.1016/j.tig.2013.01.013
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Zs.A 2272: Show issues

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Article: Our fragile intellect. Part I.

Crabtree, Gerald R

Trends in genetics : TIG

2013 Volume 29, Issue 1, Page(s) 1–3

Abstract: New developments in genetics, anthropology, and neurobiology predict that a very large number of genes underlie our intellectual and emotional abilities, making these abilities genetically surprisingly fragile. ...

Abstract	New developments in genetics, anthropology, and neurobiology predict that a very large number of genes underlie our intellectual and emotional abilities, making these abilities genetically surprisingly fragile.
MeSH term(s)	Anthropology/methods ; Anthropology/trends ; Child ; Cognition/physiology ; Cohort Effect ; Evolution, Molecular ; Fragile X Syndrome/genetics ; Genomic Instability/physiology ; Humans ; Infant, Newborn ; Intellectual Disability/genetics ; Intelligence/genetics ; Problem Solving/physiology
Language	English
Publishing date	2013-01
Publishing country	England
Document type	Journal Article
ZDB-ID	619240-3
ISSN	1362-4555 ; 0168-9525 ; 0168-9479
ISSN (online)	1362-4555
ISSN	0168-9525 ; 0168-9479
DOI	10.1016/j.tig.2012.10.002
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Article: Our fragile intellect. Part II.

Crabtree, Gerald R

Trends in genetics : TIG

2013 Volume 29, Issue 1, Page(s) 3–5

Abstract: Analysis of human mutation rates and the number of genes required for human intellectual and emotional fitness indicates that we are almost certainly losing these abilities. If so, how did we get them in the first place, and when did things begin to ... ...

Abstract	Analysis of human mutation rates and the number of genes required for human intellectual and emotional fitness indicates that we are almost certainly losing these abilities. If so, how did we get them in the first place, and when did things begin to change?
MeSH term(s)	Artificial Intelligence/trends ; Brain/anatomy & histology ; Evolution, Molecular ; Genetic Fitness/genetics ; Genetic Fitness/physiology ; Genomic Instability/physiology ; Humans ; Intelligence/genetics ; Mutation Rate ; Organ Size/genetics ; Organ Size/physiology ; Phylogeny
Language	English
Publishing date	2013-01
Publishing country	England
Document type	Journal Article
ZDB-ID	619240-3
ISSN	1362-4555 ; 0168-9525 ; 0168-9479
ISSN (online)	1362-4555
ISSN	0168-9525 ; 0168-9479
DOI	10.1016/j.tig.2012.10.003
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Article ; Online: PU.1 and BCL11B sequentially cooperate with RUNX1 to anchor mSWI/SNF to poise the T cell effector landscape.

Gamble, Noah / Bradu, Alexandra / Caldwell, Jason A / McKeever, Joshua / Bolonduro, Olubusayo / Ermis, Ebru / Kaiser, Caroline / Kim, YeEun / Parks, Benjamin / Klemm, Sandy / Greenleaf, William J / Crabtree, Gerald R / Koh, Andrew S

Nature immunology

2024 Volume 25, Issue 5, Page(s) 860–872

Abstract: Adaptive immunity relies on specialized effector functions elicited by lymphocytes, yet how antigen recognition activates appropriate effector responses through nonspecific signaling intermediates is unclear. Here we examined the role of chromatin ... ...

Abstract	Adaptive immunity relies on specialized effector functions elicited by lymphocytes, yet how antigen recognition activates appropriate effector responses through nonspecific signaling intermediates is unclear. Here we examined the role of chromatin priming in specifying the functional outputs of effector T cells and found that most of the cis-regulatory landscape active in effector T cells was poised early in development before the expression of the T cell antigen receptor. We identified two principal mechanisms underpinning this poised landscape: the recruitment of the nucleosome remodeler mammalian SWItch/Sucrose Non-Fermentable (mSWI/SNF) by the transcription factors RUNX1 and PU.1 to establish chromatin accessibility at T effector loci; and a 'relay' whereby the transcription factor BCL11B succeeded PU.1 to maintain occupancy of the chromatin remodeling complex mSWI/SNF together with RUNX1, after PU.1 silencing during lineage commitment. These mechanisms define modes by which T cells acquire the potential to elicit specialized effector functions early in their ontogeny and underscore the importance of integrating extrinsic cues to the developmentally specified intrinsic program.
MeSH term(s)	Proto-Oncogene Proteins/metabolism ; Animals ; Trans-Activators/metabolism ; Trans-Activators/genetics ; Mice ; Core Binding Factor Alpha 2 Subunit/metabolism ; Core Binding Factor Alpha 2 Subunit/genetics ; Repressor Proteins/metabolism ; Repressor Proteins/genetics ; Transcription Factors/metabolism ; Transcription Factors/genetics ; Tumor Suppressor Proteins/metabolism ; Tumor Suppressor Proteins/genetics ; Mice, Inbred C57BL ; Chromosomal Proteins, Non-Histone/metabolism ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism ; Mice, Knockout ; Chromatin Assembly and Disassembly ; Cell Differentiation/immunology
Chemical Substances	Proto-Oncogene Proteins ; proto-oncogene protein Spi-1 ; Trans-Activators ; Core Binding Factor Alpha 2 Subunit ; Repressor Proteins ; Bcl11b protein, mouse ; Transcription Factors ; Tumor Suppressor Proteins ; SWI-SNF-B chromatin-remodeling complex ; Chromosomal Proteins, Non-Histone ; Runx1 protein, mouse
Language	English
Publishing date	2024-04-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2016987-5
ISSN	1529-2916 ; 1529-2908
ISSN (online)	1529-2916
ISSN	1529-2908
DOI	10.1038/s41590-024-01807-y
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Zs.A 5294: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 42: Show issues

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Article ; Online: Author Correction: Rewiring cancer drivers to activate apoptosis.

Gourisankar, Sai / Krokhotin, Andrey / Ji, Wenzhi / Liu, Xiaofan / Chang, Chiung-Ying / Kim, Samuel H / Li, Zhengnian / Wenderski, Wendy / Simanauskaite, Juste M / Yang, Haopeng / Vogel, Hannes / Zhang, Tinghu / Green, Michael R / Gray, Nathanael S / Crabtree, Gerald R

Nature

2023 Volume 621, Issue 7977, Page(s) E27

Language	English
Publishing date	2023-08-19
Publishing country	England
Document type	Published Erratum
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/s41586-023-06543-1
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Zs.A 26: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 9: Show issues
Zs.MO 244: Show issues

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Article ; Online: Forebrain-specific conditional calcineurin deficiency induces dentate gyrus immaturity and hyper-dopaminergic signaling in mice.

Hagihara, Hideo / Shoji, Hirotaka / Kuroiwa, Mahomi / Graef, Isabella A / Crabtree, Gerald R / Nishi, Akinori / Miyakawa, Tsuyoshi

Molecular brain

2022 Volume 15, Issue 1, Page(s) 94

Abstract: Calcineurin (Cn), a phosphatase important for synaptic plasticity and neuronal development, has been implicated in the etiology and pathophysiology of neuropsychiatric disorders, including schizophrenia, intellectual disability, autism spectrum disorders, ...

Abstract	Calcineurin (Cn), a phosphatase important for synaptic plasticity and neuronal development, has been implicated in the etiology and pathophysiology of neuropsychiatric disorders, including schizophrenia, intellectual disability, autism spectrum disorders, epilepsy, and Alzheimer's disease. Forebrain-specific conditional Cn knockout mice have been known to exhibit multiple behavioral phenotypes related to these disorders. In this study, we investigated whether Cn mutant mice show pseudo-immaturity of the dentate gyrus (iDG) in the hippocampus, which we have proposed as an endophenotype shared by these disorders. Expression of calbindin and GluA1, typical markers for mature DG granule cells (GCs), was decreased and that of doublecortin, calretinin, phospho-CREB, and dopamine D1 receptor (Drd1), markers for immature GC, was increased in Cn mutants. Phosphorylation of cAMP-dependent protein kinase (PKA) substrates (GluA1, ERK2, DARPP-32, PDE4) was increased and showed higher sensitivity to SKF81297, a Drd1-like agonist, in Cn mutants than in controls. While cAMP/PKA signaling is increased in the iDG of Cn mutants, chronic treatment with rolipram, a selective PDE4 inhibitor that increases intracellular cAMP, ameliorated the iDG phenotype significantly and nesting behavior deficits with nominal significance. Chronic rolipram administration also decreased the phosphorylation of CREB, but not the other four PKA substrates examined, in Cn mutants. These results suggest that Cn deficiency induces pseudo-immaturity of GCs and that cAMP signaling increases to compensate for this maturation abnormality. This study further supports the idea that iDG is an endophenotype shared by certain neuropsychiatric disorders.
MeSH term(s)	Animals ; Mice ; Calcineurin/metabolism ; Rolipram/metabolism ; Disease Models, Animal ; Dopamine/metabolism ; Mice, Knockout ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Hippocampus/metabolism ; Dentate Gyrus/metabolism
Chemical Substances	Calcineurin (EC 3.1.3.16) ; Rolipram (K676NL63N7) ; Dopamine (VTD58H1Z2X) ; Cyclic AMP-Dependent Protein Kinases (EC 2.7.11.11)
Language	English
Publishing date	2022-11-22
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2436057-0
ISSN	1756-6606 ; 1756-6606
ISSN (online)	1756-6606
ISSN	1756-6606
DOI	10.1186/s13041-022-00981-0
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Article ; Online: CHD8 dosage regulates transcription in pluripotency and early murine neural differentiation.

Sood, Sabina / Weber, Christopher M / Hodges, H Courtney / Krokhotin, Andrey / Shalizi, Aryaman / Crabtree, Gerald R

Proceedings of the National Academy of Sciences of the United States of America

2020 Volume 117, Issue 36, Page(s) 22331–22340

Abstract: The chromatin ... ...

Abstract	The chromatin remodeler
MeSH term(s)	Animals ; Autism Spectrum Disorder ; Cells, Cultured ; Chromatin Assembly and Disassembly/genetics ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Embryonic Stem Cells/metabolism ; Gene Dosage/genetics ; Mice ; Mice, Knockout ; Neurogenesis/genetics
Chemical Substances	DNA-Binding Proteins ; duplin protein, mouse
Language	English
Publishing date	2020-08-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1921963117
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Zs.A 1148: Show issues

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Article ; Online: Chemically induced proximity in biology and medicine.

Stanton, Benjamin Z / Chory, Emma J / Crabtree, Gerald R

Science (New York, N.Y.)

2018 Volume 359, Issue 6380

Abstract: Proximity, or the physical closeness of molecules, is a pervasive regulatory mechanism in biology. For example, most posttranslational modifications such as phosphorylation, methylation, and acetylation promote proximity of molecules to play ... ...

Abstract	Proximity, or the physical closeness of molecules, is a pervasive regulatory mechanism in biology. For example, most posttranslational modifications such as phosphorylation, methylation, and acetylation promote proximity of molecules to play deterministic roles in cellular processes. To understand the role of proximity in biologic mechanisms, chemical inducers of proximity (CIPs) were developed to synthetically model biologically regulated recruitment. Chemically induced proximity allows for precise temporal control of transcription, signaling cascades, chromatin regulation, protein folding, localization, and degradation, as well as a host of other biologic processes. A systematic analysis of CIPs in basic research, coupled with recent technological advances utilizing CRISPR, distinguishes roles of causality from coincidence and allows for mathematical modeling in synthetic biology. Recently, induced proximity has provided new avenues of gene therapy and emerging advances in cancer treatment.
MeSH term(s)	Animals ; Biological Mimicry ; CRISPR-Cas Systems ; Cell- and Tissue-Based Therapy/trends ; Chromatin/chemistry ; Genetic Therapy/trends ; Humans ; Ligands ; Protein Folding ; Protein Processing, Post-Translational ; Proteins/chemistry ; Proteolysis ; Signal Transduction ; Tacrolimus/analogs & derivatives ; Tacrolimus/pharmacology ; Transcription, Genetic
Chemical Substances	Chromatin ; FK 1012 ; Ligands ; Proteins ; Tacrolimus (WM0HAQ4WNM)
Language	English
Publishing date	2018-03-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	128410-1
ISSN	1095-9203 ; 0036-8075
ISSN (online)	1095-9203
ISSN	0036-8075
DOI	10.1126/science.aao5902
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Zs.A 27: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 77: Show issues

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Article: Mammalian SWI/SNF chromatin remodeling complexes and cancer: Mechanistic insights gained from human genomics.

Kadoch, Cigall / Crabtree, Gerald R

Science advances

2015 Volume 1, Issue 5, Page(s) e1500447

Abstract: Over the past 4 years, nearly 100 exome sequencing studies have revealed the high frequency of mutations in the genes encoding the subunits of ATP-dependent chromatin remodelers in human cancer. Most of these mutations are within the genes encoding ... ...

Abstract	Over the past 4 years, nearly 100 exome sequencing studies have revealed the high frequency of mutations in the genes encoding the subunits of ATP-dependent chromatin remodelers in human cancer. Most of these mutations are within the genes encoding subunits of the BAF (Brg/Brahma-associated factors) or mSWI/SNF complex, which is one of two dozen predicted ATP-dependent chromatin remodeling complexes in mammals. Considering BAF complexes as a single entity, the 15 subunits encoded by 29 genes are mutated in >20% of human cancer, across a broad range of tumor types. These observations demonstrate that there is little redundancy in the oncogenic function of BAF complexes with the other remodeling complexes, underscoring their unique roles. Several important conclusions emerge from these genomic data: specific subunits appear to be mutated in specific cancers, highlighting tissue-specific protective roles; mutations can function as tumor suppressors or oncogenes; mutations can be homozygous or, more commonly, heterozygous, implying their dosage-sensitive roles in an unknown yet fundamental process used to suppress the genesis of cancer. These new human genetic findings paired with biochemical studies are challenging old ideas on how chromatin remodeling complexes function, generating new hypotheses with respect to their normal and oncogenic mechanisms and highlighting potential avenues for therapeutic intervention in human cancer.
Language	English
Publishing date	2015-06-12
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2810933-8
ISSN	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.1500447
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