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Article ; Online: Inflammatory Proteomic Analysis of 22q11.2 Deletion Syndrome.

Frusone, Valentina / Maurer, Kelly / Emanuel, Beverly S / McDonald-McGinn, Donna / Sullivan, Kathleen E

2024 Volume 44, Issue 3, Page(s) 82

MeSH term(s)	Humans ; DiGeorge Syndrome/diagnosis ; DiGeorge Syndrome/genetics ; Proteomics ; In Situ Hybridization, Fluorescence ; Chromosome Deletion
Language	English
Publishing date	2024-03-15
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	779361-3
ISSN	1573-2592 ; 0271-9142
ISSN (online)	1573-2592
ISSN	0271-9142
DOI	10.1007/s10875-024-01689-7
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Book ; Conference proceedings: Report of the Third International Workshop on Human Chromosome 22 Mapping 1992

Emanuel, Beverly S.

held on September 17 - 20, 1992 ... in Philadelphia, Pennsylvania

1993

Event/congress	International Workshop on Human Chromosome 22 Mapping (3, 1992, PhiladelphiaPa.)
Author's details	organized by Beverly S. Emanuel
Keywords	Chromosome Mapping / congresses ; Chromosomes, Human, Pair 22 / congresses
Language	English
Publishing country	Switzerland
Document type	Book ; Conference proceedings
Note	In: Cytogenetics and cell genetics. - ISSN 0301-0171. - 63 (1993), S. 205 - 211
HBZ-ID	HT004560799
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Article: Multiple paralogues and recombination mechanisms drive the high incidence of 22q11.2 Deletion Syndrome.

Vervoort, Lisanne / Dierckxsens, Nicolas / Santos, Marta Sousa / Meynants, Senne / Souche, Erika / Cools, Ruben / Heung, Tracy / Devriendt, Koen / Peeters, Hilde / McDonald-McGinn, Donna M / Swillen, Ann / Breckpot, Jeroen / Emanuel, Beverly S / Van Esch, Hilde / Bassett, Anne S / Vermeesch, Joris R

bioRxiv : the preprint server for biology

2024

Abstract: The 22q11.2 deletion syndrome (22q11.2DS) is the most common microdeletion disorder. Why the incidence of 22q11.2DS is much greater than that of other genomic disorders remains unknown. Short read sequencing cannot resolve the complex segmental duplicon ... ...

Abstract	The 22q11.2 deletion syndrome (22q11.2DS) is the most common microdeletion disorder. Why the incidence of 22q11.2DS is much greater than that of other genomic disorders remains unknown. Short read sequencing cannot resolve the complex segmental duplicon structure to provide direct confirmation of the hypothesis that the rearrangements are caused by non-allelic homologous recombination between the low copy repeats on chromosome 22 (LCR22s). To enable haplotype-specific assembly and rearrangement mapping in LCR22 regions, we combined fiber-FISH optical mapping with whole genome (ultra-)long read sequencing or rearrangement-specific long-range PCR on 24 duos (22q11.2DS patient and parent-of-origin) comprising several different LCR22-mediated rearrangements. Unexpectedly, we demonstrate that not only different paralogous segmental duplicon but also palindromic AT-rich repeats (PATRR) are driving 22q11.2 rearrangements. In addition, we show the existence of two different inversion polymorphisms preceding rearrangement, and somatic mosaicism. The existence of different recombination sites and mechanisms in paralogues and PATRRs which are copy number expanding in the human population are a likely explanation for the high 22q11.2DS incidence.
Language	English
Publishing date	2024-03-18
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.03.14.585046
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Article ; Online: Immunologic, Molecular, and Clinical Profile of Patients with Chromosome 22q11.2 Duplications.

Bhattarai, Dharmagat / McGinn, Daniel E / Crowley, T Blaine / Giunta, Victoria / Gaiser, Kimberly / Zackai, Elaine H / Emanuel, Beverly S / Heimall, Jennifer / Jyonouchi, Soma / Lee, Juhee / Sun, Di / McDonald-McGinn, Donna M / Sullivan, Kathleen E

Journal of clinical immunology

2023 Volume 43, Issue 4, Page(s) 794–807

Abstract: Purpose: Duplication of chromosome 22q11.2 due to meiotic non-allelic homologous recombination results in a distinct syndrome, chromosome 22q11.2 duplication syndrome that has some overlapping phenotypic features with the corresponding 22q11.2 deletion ... ...

Abstract	Purpose: Duplication of chromosome 22q11.2 due to meiotic non-allelic homologous recombination results in a distinct syndrome, chromosome 22q11.2 duplication syndrome that has some overlapping phenotypic features with the corresponding 22q11.2 deletion syndrome. Literature on immunologic aspects of the duplication syndrome is limited. We conducted a retrospective study of 216 patients with this syndrome to better define the key features of the duplication syndrome. Methods: Single-center retrospective record review was performed. Data regarding demographics, clinical details, and immunological tests were compiled, extracted into a predetermined data collection form, and analyzed. Results: This cohort comprised 113 (52.3%) males and 103 (47.7%) females. The majority (54.6%) of mapped duplications were between low copy repeat regions A-D (LCR22A to -D). Though T cell subsets were relatively preserved, switched memory B cells, immunoglobulins, and specific antibodies were each found to be decreased in a subset of the cohort. One-fifth (17/79, 21.5%) of patients had at least 2 low immunoglobulin values, and panhypogammaglobulinemia was found in 11.7% (9/79) cases. Four children were on regular immunoglobulin replacement therapy. Asthma and eczema were the predominant atopic symptoms in our cohort. Conclusion: Significant immunodeficiencies were observed in our cohort, particularly in B cells and antibodies. Our study expands the current clinical understanding and emphasizes the need of immunological studies and multidisciplinary approaches for these patients.
MeSH term(s)	Male ; Child ; Female ; Humans ; DiGeorge Syndrome/genetics ; Retrospective Studies ; Chromosome Deletion ; Syndrome ; Chromosomes
Language	English
Publishing date	2023-02-03
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	779361-3
ISSN	1573-2592 ; 0271-9142
ISSN (online)	1573-2592
ISSN	0271-9142
DOI	10.1007/s10875-023-01443-5
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Article ; Online: Psychosis spectrum features, neurocognition and functioning in a longitudinal study of youth with 22q11.2 deletion syndrome.

Gur, Raquel E / McDonald-McGinn, Donna M / Moore, Tyler M / Gallagher, R Sean / McClellan, Emily / White, Lauren / Ruparel, Kosha / Hillman, Noah / Crowley, T Blaine / McGinn, Daniel E / Zackai, Elaine / Emanuel, Beverly S / Calkins, Monica E / Roalf, David R / Gur, Ruben C

Psychological medicine

2023 , Page(s) 1–10

Abstract: Background: Neuropsychiatric disorders are common in 22q11.2 Deletion Syndrome (22q11DS) with about 25% of affected individuals developing schizophrenia spectrum disorders by young adulthood. Longitudinal evaluation of psychosis spectrum features and ... ...

Abstract	Background: Neuropsychiatric disorders are common in 22q11.2 Deletion Syndrome (22q11DS) with about 25% of affected individuals developing schizophrenia spectrum disorders by young adulthood. Longitudinal evaluation of psychosis spectrum features and neurocognition can establish developmental trajectories and impact on functional outcome. Methods: 157 youth with 22q11DS were assessed longitudinally for psychopathology focusing on psychosis spectrum symptoms, neurocognitive performance and global functioning. We contrasted the pattern of positive and negative psychosis spectrum symptoms and neurocognitive performance differentiating those with more prominent Psychosis Spectrum symptoms (PS+) to those without prominent psychosis symptoms (PS-). Results: We identified differences in the trajectories of psychosis symptoms and neurocognitive performance between the groups. The PS+ group showed age associated increase in symptom severity, especially negative symptoms and general nonspecific symptoms. Correspondingly, their level of functioning was worse and deteriorated more steeply than the PS- group. Neurocognitive performance was generally comparable in PS+ and PS- groups and demonstrated a similar age-related trajectory. However, worsening executive functioning distinguished the PS+ group from PS- counterparts. Notably, of the three executive function measures examined, only working memory showed a significant difference between the groups in rate of change. Finally, structural equation modeling showed that neurocognitive decline drove the clinical change. Conclusions: Youth with 22q11DS and more prominent psychosis features show worsening of symptoms and functional decline driven by neurocognitive decline, most related to executive functions and specifically working memory. The results underscore the importance of working memory in the developmental progression of psychosis.
Language	English
Publishing date	2023-03-29
Publishing country	England
Document type	Journal Article
ZDB-ID	217420-0
ISSN	1469-8978 ; 0033-2917
ISSN (online)	1469-8978
ISSN	0033-2917
DOI	10.1017/S0033291723000259
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Article: A Novel Non-Allelic Homologous Recombination Event in a Parent with an 11;22 Reciprocal Translocation Leading to 22q11.2 Deletion Syndrome

Pastor, Steven / Tran, Oanh / McGinn, Daniel E. / Crowley, T. Blaine / Zackai, Elaine H. / McDonald-McGinn, Donna M. / Emanuel, Beverly S.

Genes. 2022 Sept. 17, v. 13, no. 9

2022

Abstract: ... homologous recombination (NAHR) mediated by the LCR22s. The ability to fully delineate an individual’s 22q11.2 ... regional structure will likely be important for studies designed to assess an unaffected individual’s risk ... deletion in his affected child. The unaffected sibling of the proband with 22q11.2DS inherited the father’s ...

Abstract	The most prevalent microdeletion in the human population occurs at 22q11.2, a region rich in chromosome-specific low copy repeats (LCR22s). The structure of this region has eluded characterization due to a combination of size, regional complexity, and haplotype diversity. To further complicate matters, it is not well represented in the human reference genome. Most individuals with 22q11.2 deletion syndrome (22q11.2DS) carry a de novo, hemizygous deletion approximately 3 Mbp in size occurring by non-allelic homologous recombination (NAHR) mediated by the LCR22s. The ability to fully delineate an individual’s 22q11.2 regional structure will likely be important for studies designed to assess an unaffected individual’s risk for generating rearrangements in germ cells, potentially leading to offspring with 22q11.2DS. Towards understanding these risk factors, optical mapping has been previously employed to successfully elucidate the structure and variation of LCR22s across 30 families affected by 22q11.2DS. The father in one of these families carries a t(11;22)(q23;q11) translocation. Surprisingly, it was determined that he is the parent-of-deletion-origin. NAHR, which occurred between his der(22) and intact chromosome 22, led to a 22q11.2 deletion in his affected child. The unaffected sibling of the proband with 22q11.2DS inherited the father’s normal chromosome 22, which did not aberrantly recombine. This unexpected observation definitively shows that haplotypes that engage in NAHR can also be inherited intact. This study is the first to identify all structures involving a rearranged chromosome 22 that also participates in NAHR leading to a 22q11.2 deletion.
Keywords	children ; chromosomes ; genome ; haplotypes ; homologous recombination ; human population ; humans ; reciprocal translocation ; risk
Language	English
Dates of publication	2022-0917
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2527218-4
ISSN	2073-4425
ISSN	2073-4425
DOI	10.3390/genes13091668
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: A Novel Non-Allelic Homologous Recombination Event in a Parent with an 11;22 Reciprocal Translocation Leading to 22q11.2 Deletion Syndrome.

Pastor, Steven / Tran, Oanh / McGinn, Daniel E / Crowley, T Blaine / Zackai, Elaine H / McDonald-McGinn, Donna M / Emanuel, Beverly S

Genes

2022 Volume 13, Issue 9

Abstract: The most prevalent microdeletion in the human population occurs at 22q11.2, a region rich in chromosome-specific low copy repeats (LCR22s). The structure of this region has eluded characterization due to a combination of size, regional complexity, and ... ...

Abstract	The most prevalent microdeletion in the human population occurs at 22q11.2, a region rich in chromosome-specific low copy repeats (LCR22s). The structure of this region has eluded characterization due to a combination of size, regional complexity, and haplotype diversity. To further complicate matters, it is not well represented in the human reference genome. Most individuals with 22q11.2 deletion syndrome (22q11.2DS) carry a de novo, hemizygous deletion approximately 3 Mbp in size occurring by non-allelic homologous recombination (NAHR) mediated by the LCR22s. The ability to fully delineate an individual's 22q11.2 regional structure will likely be important for studies designed to assess an unaffected individual's risk for generating rearrangements in germ cells, potentially leading to offspring with 22q11.2DS. Towards understanding these risk factors, optical mapping has been previously employed to successfully elucidate the structure and variation of LCR22s across 30 families affected by 22q11.2DS. The father in one of these families carries a t(11;22)(q23;q11) translocation. Surprisingly, it was determined that he is the parent-of-deletion-origin. NAHR, which occurred between his der(22) and intact chromosome 22, led to a 22q11.2 deletion in his affected child. The unaffected sibling of the proband with 22q11.2DS inherited the father's normal chromosome 22, which did not aberrantly recombine. This unexpected observation definitively shows that haplotypes that engage in NAHR can also be inherited intact. This study is the first to identify all structures involving a rearranged chromosome 22 that also participates in NAHR leading to a 22q11.2 deletion.
MeSH term(s)	Alleles ; Child ; DiGeorge Syndrome/genetics ; Homologous Recombination/genetics ; Humans ; Male ; Parents ; Segmental Duplications, Genomic ; Translocation, Genetic/genetics
Language	English
Publishing date	2022-09-17
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2527218-4
ISSN	2073-4425 ; 2073-4425
ISSN (online)	2073-4425
ISSN	2073-4425
DOI	10.3390/genes13091668
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Article: Molecular mechanisms and diagnosis of chromosome 22q11.2 rearrangements.

Emanuel, Beverly S

Developmental disabilities research reviews

2008 Volume 14, Issue 1, Page(s) 11–18

Abstract: ... that give rise to the recurrent t(11;22) supernumerary der(22) syndrome (Emanuel syndrome ...

Abstract	Several recurrent, constitutional genomic disorders are present on chromosome 22q. These include the translocations and deletions associated with DiGeorge and velocardiofacial syndrome and the translocations that give rise to the recurrent t(11;22) supernumerary der(22) syndrome (Emanuel syndrome). The rearrangement breakpoints on 22q cluster around the chromosome-specific segmental duplications of proximal 22q11, which are involved in the etiology of these disorders. While the deletions are the result of nonallelic homologous recombination (NAHR) between low copy repeats or segmental duplications within 22q11, the t(11;22) is the result of rearrangement between palindromic AT-rich repeats on 11q and 22q. Here we describe the mechanisms responsible for these recurrent rearrangements, discuss the recurrent deletion endpoints that are the result of NAHR between chromosome 22q specific low copy repeats as well as present current diagnostic approaches to deletion detection.
MeSH term(s)	Child ; Chromosome Breakage ; Chromosome Deletion ; Chromosomes, Human, Pair 22/genetics ; DiGeorge Syndrome/diagnosis ; DiGeorge Syndrome/genetics ; Gene Duplication ; Gene Rearrangement/genetics ; Genotype ; Humans ; Oligonucleotide Array Sequence Analysis ; Phenotype ; Repetitive Sequences, Nucleic Acid ; Translocation, Genetic
Language	English
Publishing date	2008-07-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2421523-5
ISSN	1940-5529 ; 1940-5510
ISSN (online)	1940-5529
ISSN	1940-5510
DOI	10.1002/ddrr.3
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Article ; Online: Gastrointestinal Features of 22q11.2 Deletion Syndrome Include Chronic Motility Problems From Childhood to Adulthood.

Kotcher, Rebecca E / Chait, Daniel B / Heckert, Jason M / Crowley, T Blaine / Forde, Kimberly A / Ahuja, Nitin K / Mascarenhas, Maria R / Emanuel, Beverly S / Zackai, Elaine H / McDonald-McGinn, Donna M / Reynolds, James C

Journal of pediatric gastroenterology and nutrition

2022 Volume 75, Issue 2, Page(s) e8–e14

Abstract: Objectives: 22q11.2 deletion syndrome (22q11.2DS) is the most common chromosomal microdeletion syndrome and has a multisystemic presentation including gastrointestinal features that have not yet been fully described. Our aim was to examine lifetime ... ...

Abstract	Objectives: 22q11.2 deletion syndrome (22q11.2DS) is the most common chromosomal microdeletion syndrome and has a multisystemic presentation including gastrointestinal features that have not yet been fully described. Our aim was to examine lifetime gastrointestinal problems in a large cohort of patients with 22q11.2DS. Methods: All patients followed in the 22q and You Center at the Children's Hospital of Philadelphia (n = 1421) were retrospectively screened for: 1) age ≥ 17 years, 2) documented chromosomal microdeletion within the 22q11.2 LCR22A-LCR22D region, and 3) sufficient clinical data to characterize the adult gastrointestinal phenotype. Gastrointestinal problems in childhood, adolescence, and adulthood were summarized. Statistical association testing of symptoms against other patient characteristics was performed. Results: Included patients (n = 206; 46% female; mean age, 27 years; median follow-up, 21 years) had similar clinical characteristics to the overall cohort. Genetic distribution was also similar, with 96% having deletions including the critical LCR22A-LCR22B segment (95% in the overall cohort). Most patients experienced chronic gastrointestinal symptoms in their lifetime (91%), but congenital gastrointestinal malformations (3.5%) and gastrointestinal autoimmune diseases (1.5%) were uncommon. Chronic symptoms without anatomic or pathologic abnormalities represented the vast burden of illness. Chronic symptoms in adulthood are associated with other chronic gastrointestinal symptoms and psychiatric comorbidities ( P < 0.01) but not with deletion size or physiologic comorbidities ( P > 0.05). One exception was increased nausea/vomiting in hypothyroidism ( P = 0.002). Conclusions: Functional gastrointestinal disorders (FGIDs) are a common cause of ill health in children and adults with 22q11.2DS. Providers should consider screening for the deletion in patients presenting with FGIDs and associated comorbidities such as neuropsychiatric illness, congenital heart disease, and palatal abnormalities.
MeSH term(s)	Comorbidity ; DiGeorge Syndrome/complications ; DiGeorge Syndrome/genetics ; Female ; Gastrointestinal Diseases/complications ; Gastrointestinal Diseases/genetics ; Heart Defects, Congenital ; Humans ; Male ; Phenotype ; Retrospective Studies
Language	English
Publishing date	2022-06-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	603201-1
ISSN	1536-4801 ; 0277-2116
ISSN (online)	1536-4801
ISSN	0277-2116
DOI	10.1097/MPG.0000000000003491
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Article ; Online: Rare coding variants as risk modifiers of the 22q11.2 deletion implicate postnatal cortical development in syndromic schizophrenia.

Molecular psychiatry

2023 Volume 28, Issue 5, Page(s) 2071–2080

Abstract: 22q11.2 deletion is one of the strongest known genetic risk factors for schizophrenia. Recent whole-genome sequencing of schizophrenia cases and controls with this deletion provided an unprecedented opportunity to identify risk modifying genetic variants ...

Abstract	22q11.2 deletion is one of the strongest known genetic risk factors for schizophrenia. Recent whole-genome sequencing of schizophrenia cases and controls with this deletion provided an unprecedented opportunity to identify risk modifying genetic variants and investigate their contribution to the pathogenesis of schizophrenia in 22q11.2 deletion syndrome. Here, we apply a novel analytic framework that integrates gene network and phenotype data to investigate the aggregate effects of rare coding variants and identified modifier genes in this etiologically homogenous cohort (223 schizophrenia cases and 233 controls of European descent). Our analyses revealed significant additive genetic components of rare nonsynonymous variants in 110 modifier genes (adjusted P = 9.4E-04) that overall accounted for 4.6% of the variance in schizophrenia status in this cohort, of which 4.0% was independent of the common polygenic risk for schizophrenia. The modifier genes affected by rare coding variants were enriched with genes involved in synaptic function and developmental disorders. Spatiotemporal transcriptomic analyses identified an enrichment of coexpression between modifier and 22q11.2 genes in cortical brain regions from late infancy to young adulthood. Corresponding gene coexpression modules are enriched with brain-specific protein-protein interactions of SLC25A1, COMT, and PI4KA in the 22q11.2 deletion region. Overall, our study highlights the contribution of rare coding variants to the SCZ risk. They not only complement common variants in disease genetics but also pinpoint brain regions and developmental stages critical to the etiology of syndromic schizophrenia.
MeSH term(s)	Humans ; Young Adult ; Adult ; Schizophrenia/genetics ; DiGeorge Syndrome/genetics ; Brain ; Gene Expression Profiling ; Whole Genome Sequencing
Language	English
Publishing date	2023-03-03
Publishing country	England
Document type	Journal Article
ZDB-ID	1330655-8
ISSN	1476-5578 ; 1359-4184
ISSN (online)	1476-5578
ISSN	1359-4184
DOI	10.1038/s41380-023-02009-y
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