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Article ; Online: Cryopreservation of C. elegans and Other Nematodes with Dimethyl Sulfoxide and Trehalose.

O'Connell, Kevin F

Methods in molecular biology (Clifton, N.J.)

2022 Volume 2468, Page(s) 43–49

Abstract: One of the key attributes that has contributed to the popularity of Caenorhabditis elegans as a model system is its ability to survive freezing. By preserving stocks at ultralow temperature, researchers have been able to generate an unlimited number of ... ...

Abstract	One of the key attributes that has contributed to the popularity of Caenorhabditis elegans as a model system is its ability to survive freezing. By preserving stocks at ultralow temperature, researchers have been able to generate an unlimited number of strains without the burden of constantly maintaining them. This has facilitated the use of large-scale forward genetic screens and CRISPR-mediated genome editing where large numbers of novel and informative mutants can be generated. Traditionally, C. elegans and other nematodes were frozen using glycerol as a cryoprotectant. While effective, a large majority of animals do not survive a typical freeze-thaw cycle. Here I describe an alternative method based on the popular combination of DMSO and trehalose as a cryoprotectant. This method allows the survival of large numbers of worms and effectively protects most developmental stages including adults.
MeSH term(s)	Animals ; Caenorhabditis elegans/genetics ; Cryopreservation/methods ; Cryoprotective Agents/pharmacology ; Dimethyl Sulfoxide/pharmacology ; Trehalose
Chemical Substances	Cryoprotective Agents ; Trehalose (B8WCK70T7I) ; Dimethyl Sulfoxide (YOW8V9698H)
Language	English
Publishing date	2022-03-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-2181-3_3
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Article ; Online: Centrosomes: An acentriolar MTOC at the ciliary base.

O'Connell, Kevin F

Current biology : CB

2021 Volume 31, Issue 11, Page(s) R730–R733

Abstract: Centrioles are microtubule-based organelles that are embedded within pericentriolar material (PCM). Together, they comprise the centrosome, a microtubule-organizing center. PCM can sometimes exist in the absence of centrioles, but a new example of ... ...

Abstract	Centrioles are microtubule-based organelles that are embedded within pericentriolar material (PCM). Together, they comprise the centrosome, a microtubule-organizing center. PCM can sometimes exist in the absence of centrioles, but a new example of acentriolar PCM in neurons offers deeper insight into the relationship between these two entities.
MeSH term(s)	Centrioles ; Centrosome ; Cilia ; Microtubule-Organizing Center ; Microtubules
Language	English
Publishing date	2021-07-05
Publishing country	England
Document type	Journal Article ; Comment
ZDB-ID	1071731-6
ISSN	1879-0445 ; 0960-9822
ISSN (online)	1879-0445
ISSN	0960-9822
DOI	10.1016/j.cub.2021.03.101
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Article ; Online: An in vitro neurogenetics platform for precision disease modeling in the mouse.

Cortes, Daniel E / Escudero, Mélanie / Korgan, Austin C / Mitra, Arojit / Edwards, Alyssa / Aydin, Selcan C / Munger, Steven C / Charland, Kevin / Zhang, Zhong-Wei / O'Connell, Kristen M S / Reinholdt, Laura G / Pera, Martin F

Science advances

2024 Volume 10, Issue 14, Page(s) eadj9305

Abstract: The power and scope of disease modeling can be markedly enhanced through the incorporation of broad genetic diversity. The introduction of pathogenic mutations into a single inbred mouse strain sometimes fails to mimic human disease. We describe a cross- ... ...

Abstract	The power and scope of disease modeling can be markedly enhanced through the incorporation of broad genetic diversity. The introduction of pathogenic mutations into a single inbred mouse strain sometimes fails to mimic human disease. We describe a cross-species precision disease modeling platform that exploits mouse genetic diversity to bridge cell-based modeling with whole organism analysis. We developed a universal protocol that permitted robust and reproducible neural differentiation of genetically diverse human and mouse pluripotent stem cell lines and then carried out a proof-of-concept study of the neurodevelopmental gene
MeSH term(s)	Animals ; Mice ; Humans ; Pluripotent Stem Cells ; Phenotype
Language	English
Publishing date	2024-04-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.adj9305
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Article: Identification of Novel Genomic Loci for Anxiety and Extensive Genetic Overlap with Psychiatric Disorders.

Tesfaye, Markos / Jaholkowski, Piotr / Shadrin, Alexey A / van der Meer, Dennis / Hindley, Guy F L / Holen, Børge / Parker, Nadine / Parekh, Pravesh / Birkenæs, Viktoria / Rahman, Zillur / Bahrami, Shahram / Kutrolli, Gleda / Frei, Oleksandr / Djurovic, Srdjan / Dale, Anders M / Smeland, Olav B / O'Connell, Kevin S / Andreassen, Ole A

medRxiv : the preprint server for health sciences

2024

Abstract: Background: Anxiety disorders are prevalent and anxiety symptoms co-occur with many psychiatric disorders. We aimed to identify genomic risk loci associated with anxiety, characterize its genetic architecture, and genetic overlap with psychiatric ... ...

Abstract	Background: Anxiety disorders are prevalent and anxiety symptoms co-occur with many psychiatric disorders. We aimed to identify genomic risk loci associated with anxiety, characterize its genetic architecture, and genetic overlap with psychiatric disorders. Methods: We used the GWAS of anxiety symptoms, schizophrenia, bipolar disorder, major depression, and attention deficit hyperactivity disorder (ADHD). We employed MiXeR and LAVA to characterize the genetic architecture and genetic overlap between the phenotypes. Conditional and conjunctional false discovery rate analyses were performed to boost the identification of genomic loci associated with anxiety and those shared with psychiatric disorders. Gene annotation and gene set analyses were conducted using OpenTargets and FUMA, respectively. Results: Anxiety was polygenic with 12.9k estimated genetic risk variants and overlapped extensively with psychiatric disorders (4.1-11.4k variants). MiXeR and LAVA revealed predominantly positive genetic correlations between anxiety and psychiatric disorders. We identified 114 novel loci for anxiety by conditioning on the psychiatric disorders. We also identified loci shared between anxiety and major depression ( Conclusions: Anxiety is a highly polygenic phenotype with extensive genetic overlap with psychiatric disorders. These genetic overlaps enabled the identification of novel loci for anxiety. The shared genetic architecture may underlie the extensive cross-disorder comorbidity of anxiety, and the identified genetic loci implicate molecular pathways that may lead to potential drug targets.
Language	English
Publishing date	2024-04-08
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.09.01.23294920
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Article ; Online: CDK-11-Cyclin L is required for gametogenesis and fertility in C. elegans.

Williams, Christopher W / Iyer, Jyoti / Liu, Yan / O'Connell, Kevin F

Developmental biology

2018 Volume 441, Issue 1, Page(s) 52–66

Abstract: CDK11, a member of the cyclin-dependent kinase family, has been implicated in a diverse array of functions including transcription, RNA processing, sister chromatid cohesion, spindle assembly, centriole duplication and apoptosis. Despite its involvement ... ...

Abstract	CDK11, a member of the cyclin-dependent kinase family, has been implicated in a diverse array of functions including transcription, RNA processing, sister chromatid cohesion, spindle assembly, centriole duplication and apoptosis. Despite its involvement in many essential functions, little is known about the requirements for CDK11 and its partner Cyclin L in a developing multicellular organism. Here we investigate the function of CDK11 and Cyclin L during development of the nematode Caenorhabditis elegans. Worms express two CDK11 proteins encoded by distinct loci: CDK-11.1 is essential for normal male and female fertility and is broadly expressed in the nuclei of somatic and germ line cells, while CDK-11.2 is nonessential and is enriched in hermaphrodite germ line nuclei beginning in mid pachytene. Hermaphrodites lacking CDK-11.1 develop normally but possess fewer mature sperm and oocytes and do not fully activate the RAS-ERK pathway that is required for oocyte production in response to environmental cues. Most of the sperm and eggs that are produced in cdk-11.1 null animals appear to complete development normally but fail to engage in sperm-oocyte signaling suggesting that CDK-11.1 is needed at multiple points in gametogenesis. Finally, we find that CDK-11.1 and CDK-11.2 function redundantly during embryonic and postembryonic development and likely do so in association with Cyclin L. Our results thus define multiple requirements for CDK-11-Cyclin L during animal development.
MeSH term(s)	Animals ; Caenorhabditis elegans/embryology ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans Proteins/genetics ; Caenorhabditis elegans Proteins/metabolism ; Cyclin-Dependent Kinases/genetics ; Cyclin-Dependent Kinases/metabolism ; Cyclins/genetics ; Cyclins/metabolism ; Female ; Fertility/physiology ; Male ; Oogenesis/physiology ; Spermatogenesis/physiology
Chemical Substances	Caenorhabditis elegans Proteins ; Cyclins ; Cyclin-Dependent Kinases (EC 2.7.11.22)
Language	English
Publishing date	2018-06-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
ZDB-ID	1114-9
ISSN	1095-564X ; 0012-1606
ISSN (online)	1095-564X
ISSN	0012-1606
DOI	10.1016/j.ydbio.2018.06.006
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Article ; Online: Identification of novel genomic risk loci shared between common epilepsies and psychiatric disorders.

Karadag, Naz / Shadrin, Alexey A / O'Connell, Kevin S / Hindley, Guy F L / Rahman, Zillur / Parker, Nadine / Bahrami, Shahram / Fominykh, Vera / Cheng, Weiqiu / Holen, Børge / Alvestad, Silje / Taubøll, Erik / Steen, Nils Eiel / Djurovic, Srdjan / Dale, Anders M / Frei, Oleksandr / Andreassen, Ole A / Smeland, Olav B

Brain : a journal of neurology

2023 Volume 146, Issue 8, Page(s) 3392–3403

Abstract: Psychiatric disorders and common epilepsies are heritable disorders with a high comorbidity and overlapping symptoms. However, the causative mechanisms underlying this relationship are poorly understood. Here we aimed to identify overlapping genetic loci ...

Abstract	Psychiatric disorders and common epilepsies are heritable disorders with a high comorbidity and overlapping symptoms. However, the causative mechanisms underlying this relationship are poorly understood. Here we aimed to identify overlapping genetic loci between epilepsy and psychiatric disorders to gain a better understanding of their comorbidity and shared clinical features. We analysed genome-wide association study data for all epilepsies (n = 44 889), genetic generalized epilepsy (n = 33 446), focal epilepsy (n = 39 348), schizophrenia (n = 77 096), bipolar disorder (n = 406 405), depression (n = 500 199), attention deficit hyperactivity disorder (n = 53 293) and autism spectrum disorder (n = 46 350). First, we applied the MiXeR tool to estimate the total number of causal variants influencing the disorders. Next, we used the conjunctional false discovery rate statistical framework to improve power to discover shared genomic loci. Additionally, we assessed the validity of the findings in independent cohorts, and functionally characterized the identified loci. The epilepsy phenotypes were considerably less polygenic (1.0 K to 3.4 K causal variants) than the psychiatric disorders (5.6 K to 13.9 K causal variants), with focal epilepsy being the least polygenic (1.0 K variants), and depression having the highest polygenicity (13.9 K variants). We observed cross-trait genetic enrichment between genetic generalized epilepsy and all psychiatric disorders and between all epilepsies and schizophrenia and depression. Using conjunctional false discovery rate analysis, we identified 40 distinct loci jointly associated with epilepsies and psychiatric disorders at conjunctional false discovery rate <0.05, four of which were associated with all epilepsies and 39 with genetic generalized epilepsy. Most epilepsy risk loci were shared with schizophrenia (n = 31). Among the identified loci, 32 were novel for genetic generalized epilepsy, and two were novel for all epilepsies. There was a mixture of concordant and discordant allelic effects in the shared loci. The sign concordance of the identified variants was highly consistent between the discovery and independent datasets for all disorders, supporting the validity of the findings. Gene-set analysis for the shared loci between schizophrenia and genetic generalized epilepsy implicated biological processes related to cell cycle regulation, protein phosphatase activity, and membrane and vesicle function; the gene-set analyses for the other loci were underpowered. The extensive genetic overlap with mixed effect directions between psychiatric disorders and common epilepsies demonstrates a complex genetic relationship between these disorders, in line with their bi-directional relationship, and indicates that overlapping genetic risk may contribute to shared pathophysiological and clinical features between epilepsy and psychiatric disorders.
MeSH term(s)	Humans ; Autism Spectrum Disorder/genetics ; Genome-Wide Association Study ; Attention Deficit Disorder with Hyperactivity ; Epilepsies, Partial/genetics ; Genomics ; Epilepsy, Generalized/genetics ; Genetic Loci/genetics ; Genetic Predisposition to Disease/genetics ; Polymorphism, Single Nucleotide/genetics
Language	English
Publishing date	2023-02-10
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80072-7
ISSN	1460-2156 ; 0006-8950
ISSN (online)	1460-2156
ISSN	0006-8950
DOI	10.1093/brain/awad038
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Article ; Online: Shared genetic architecture between irritable bowel syndrome and psychiatric disorders reveals molecular pathways of the gut-brain axis.

Tesfaye, Markos / Jaholkowski, Piotr / Hindley, Guy F L / Shadrin, Alexey A / Rahman, Zillur / Bahrami, Shahram / Lin, Aihua / Holen, Børge / Parker, Nadine / Cheng, Weiqiu / Rødevand, Linn / Frei, Oleksandr / Djurovic, Srdjan / Dale, Anders M / Smeland, Olav B / O'Connell, Kevin S / Andreassen, Ole A

Genome medicine

2023 Volume 15, Issue 1, Page(s) 60

Abstract: Background: Irritable bowel syndrome (IBS) often co-occurs with psychiatric and gastrointestinal disorders. A recent genome-wide association study (GWAS) identified several genetic risk variants for IBS. However, most of the heritability remains ... ...

Abstract	Background: Irritable bowel syndrome (IBS) often co-occurs with psychiatric and gastrointestinal disorders. A recent genome-wide association study (GWAS) identified several genetic risk variants for IBS. However, most of the heritability remains unidentified, and the genetic overlap with psychiatric and somatic disorders is not quantified beyond genome-wide genetic correlations. Here, we characterize the genetic architecture of IBS, further, investigate its genetic overlap with psychiatric and gastrointestinal phenotypes, and identify novel genomic risk loci. Methods: Using GWAS summary statistics of IBS (53,400 cases and 433,201 controls), and psychiatric and gastrointestinal phenotypes, we performed bivariate casual mixture model analysis to characterize the genetic architecture and genetic overlap between these phenotypes. We leveraged identified genetic overlap to boost the discovery of genomic loci associated with IBS, and to identify specific shared loci associated with both IBS and psychiatric and gastrointestinal phenotypes, using the conditional/conjunctional false discovery rate (condFDR/conjFDR) framework. We used functional mapping and gene annotation (FUMA) for functional analyses. Results: IBS was highly polygenic with 12k trait-influencing variants. We found extensive polygenic overlap between IBS and psychiatric disorders and to a lesser extent with gastrointestinal diseases. We identified 132 independent IBS-associated loci (condFDR < 0.05) by conditioning on psychiatric disorders (n = 127) and gastrointestinal diseases (n = 24). Using conjFDR, 70 unique loci were shared between IBS and psychiatric disorders. Functional analyses of shared loci revealed enrichment for biological pathways of the nervous and immune systems. Genetic correlations and shared loci between psychiatric disorders and IBS subtypes were different. Conclusions: We found extensive polygenic overlap of IBS and psychiatric and gastrointestinal phenotypes beyond what was revealed with genetic correlations. Leveraging the overlap, we discovered genetic loci associated with IBS which implicate a wide range of biological pathways beyond the gut-brain axis. Genetic differences may underlie the clinical subtype of IBS. These results increase our understanding of the pathophysiology of IBS which may form the basis for the development of individualized interventions.
MeSH term(s)	Humans ; Irritable Bowel Syndrome/genetics ; Irritable Bowel Syndrome/complications ; Brain-Gut Axis ; Genome-Wide Association Study ; Mental Disorders/genetics ; Gastrointestinal Diseases ; Polymorphism, Single Nucleotide ; Genetic Predisposition to Disease
Language	English
Publishing date	2023-08-01
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2484394-5
ISSN	1756-994X ; 1756-994X
ISSN (online)	1756-994X
ISSN	1756-994X
DOI	10.1186/s13073-023-01212-4
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Article: Revisiting Centrioles in Nematodes-Historic Findings and Current Topics.

Schwarz, Anna / Sankaralingam, Prabhu / O'Connell, Kevin F / Müller-Reichert, Thomas

Cells

2018 Volume 7, Issue 8

Abstract: Theodor Boveri is considered as the "father" of centrosome biology. Boveri's fundamental findings have laid the groundwork for decades of research on centrosomes. Here, we briefly review his early work on centrosomes and his first description of the ... ...

Abstract	Theodor Boveri is considered as the "father" of centrosome biology. Boveri's fundamental findings have laid the groundwork for decades of research on centrosomes. Here, we briefly review his early work on centrosomes and his first description of the centriole. Mainly focusing on centriole structure, duplication, and centriole assembly factors in
Language	English
Publishing date	2018-08-08
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2661518-6
ISSN	2073-4409
ISSN	2073-4409
DOI	10.3390/cells7080101
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Article ; Online: The chromatin remodeling protein CHD-1 and the EFL-1/DPL-1 transcription factor cooperatively down regulate CDK-2 to control SAS-6 levels and centriole number.

Iyer, Jyoti / Gentry, Lindsey K / Bergwell, Mary / Smith, Amy / Guagliardo, Sarah / Kropp, Peter A / Sankaralingam, Prabhu / Liu, Yan / Spooner, Eric / Bowerman, Bruce / O'Connell, Kevin F

PLoS genetics

2022 Volume 18, Issue 4, Page(s) e1009799

Abstract: Centrioles are submicron-scale, barrel-shaped organelles typically found in pairs, and play important roles in ciliogenesis and bipolar spindle assembly. In general, successful execution of centriole-dependent processes is highly reliant on the ability ... ...

Abstract	Centrioles are submicron-scale, barrel-shaped organelles typically found in pairs, and play important roles in ciliogenesis and bipolar spindle assembly. In general, successful execution of centriole-dependent processes is highly reliant on the ability of the cell to stringently control centriole number. This in turn is mainly achieved through the precise duplication of centrioles during each S phase. Aberrations in centriole duplication disrupt spindle assembly and cilia-based signaling and have been linked to cancer, primary microcephaly and a variety of growth disorders. Studies aimed at understanding how centriole duplication is controlled have mainly focused on the post-translational regulation of two key components of this pathway: the master regulatory kinase ZYG-1/Plk4 and the scaffold component SAS-6. In contrast, how transcriptional control mechanisms might contribute to this process have not been well explored. Here we show that the chromatin remodeling protein CHD-1 contributes to the regulation of centriole duplication in the C. elegans embryo. Specifically, we find that loss of CHD-1 or inactivation of its ATPase activity can restore embryonic viability and centriole duplication to a strain expressing insufficient ZYG-1 activity. Interestingly, loss of CHD-1 is associated with increases in the levels of two ZYG-1-binding partners: SPD-2, the centriole receptor for ZYG-1 and SAS-6. Finally, we explore transcriptional regulatory networks governing centriole duplication and find that CHD-1 and a second transcription factor, EFL-1/DPL-1 cooperate to down regulate expression of CDK-2, which in turn promotes SAS-6 protein levels. Disruption of this regulatory network results in the overexpression of SAS-6 and the production of extra centrioles.
MeSH term(s)	Animals ; Caenorhabditis elegans/metabolism ; Caenorhabditis elegans Proteins/genetics ; Caenorhabditis elegans Proteins/metabolism ; Cell Cycle Proteins/genetics ; Centrioles/genetics ; Centrioles/metabolism ; Chromatin Assembly and Disassembly/genetics ; Protein Kinases/genetics ; Transcription Factors/genetics ; Transcription Factors/metabolism
Chemical Substances	Caenorhabditis elegans Proteins ; Cell Cycle Proteins ; SAS-6 protein, C elegans ; Transcription Factors ; Protein Kinases (EC 2.7.-) ; zyg-1 protein, C elegans (EC 2.7.1.-)
Language	English
Publishing date	2022-04-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Research Support, N.I.H., Extramural
ZDB-ID	2186725-2
ISSN	1553-7404 ; 1553-7390
ISSN (online)	1553-7404
ISSN	1553-7390
DOI	10.1371/journal.pgen.1009799
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Article ; Online: How Real-World Data Can Facilitate the Development of Precision Medicine Treatment in Psychiatry.

Koch, Elise / Pardiñas, Antonio F / O'Connell, Kevin S / Selvaggi, Pierluigi / Camacho Collados, José / Babic, Aleksandar / Marshall, Serena E / Van der Eycken, Erik / Angulo, Cecilia / Lu, Yi / Sullivan, Patrick F / Dale, Anders M / Molden, Espen / Posthuma, Danielle / White, Nathan / Schubert, Alexander / Djurovic, Srdjan / Heimer, Hakon / Stefánsson, Hreinn /

Stefánsson, Kári / Werge, Thomas / Sønderby, Ida / O'Donovan, Michael C / Walters, James T R / Milani, Lili / Andreassen, Ole A

Biological psychiatry

2024

Abstract: Precision medicine has the ambition to improve treatment response and clinical outcomes through patient stratification and holds great potential for the treatment of mental disorders. However, several important factors are needed to transform current ... ...

Abstract	Precision medicine has the ambition to improve treatment response and clinical outcomes through patient stratification and holds great potential for the treatment of mental disorders. However, several important factors are needed to transform current practice into a precision psychiatry framework. Most important are 1) the generation of accessible large real-world training and test data including genomic data integrated from multiple sources, 2) the development and validation of advanced analytical tools for stratification and prediction, and 3) the development of clinically useful management platforms for patient monitoring that can be integrated into health care systems in real-life settings. This narrative review summarizes strategies for obtaining the key elements-well-powered samples from large biobanks integrated with electronic health records and health registry data using novel artificial intelligence algorithms-to predict outcomes in severe mental disorders and translate these models into clinical management and treatment approaches. Key elements are massive mental health data and novel artificial intelligence algorithms. For the clinical translation of these strategies, we discuss a precision medicine platform for improved management of mental disorders. We use cases to illustrate how precision medicine interventions could be brought into psychiatry to improve the clinical outcomes of mental disorders.
Language	English
Publishing date	2024-01-05
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	209434-4
ISSN	1873-2402 ; 0006-3223
ISSN (online)	1873-2402
ISSN	0006-3223
DOI	10.1016/j.biopsych.2024.01.001
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