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Cited by 257Genomic variations and chromosomal abnormalitiesGenetic Syndromes and ImprintingGenetics and Neurodevelopmental Disorders

Microdeletion/microduplication of proximal 15q11.2 between BP1 and BP2: A susceptibility region for neurological dysfunction including developmental and language delay

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Burnside, Rachel D., Pasion, Romela, Mikhail, Fady M., Carroll, Andrew J., Robin, Nathaniel H., Youngs, Erin L., Gadi, Inder K., Keitges, Elizabeth +9 more·2011·Human Genetics
DOI 10.1007/s00439-011-0970-4PMC PMC6814187
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Abstract

The proximal long arm of chromosome 15 has segmental duplications located at breakpoints BP1-BP5 that mediate the generation of NAHR-related microdeletions and microduplications. The classical Prader-Willi/Angelman syndrome deletion is flanked by either of the proximal BP1 or BP2 breakpoints and the distal BP3 breakpoint. The larger Type I deletions are flanked by BP1 and BP3 in both Prader-Willi and Angelman syndrome subjects. Those with this deletion are reported to have a more severe phenotype than individuals with either Type II deletions (BP2-BP3) or uniparental disomy 15. The BP1-BP2 region spans approximately 500 kb and contains four evolutionarily conserved genes that are not imprinted. Reports of mutations or disturbed expression of these genes appear to impact behavioral and neurological function in affected individuals. Recently, reports of deletions and duplications flanked by BP1 and BP2 suggest an association with speech and motor delays, behavioral problems, seizures, and autism. We present a large cohort of subjects with copy number alteration of BP1 to BP2 with common phenotypic features. These include autism, developmental delay, motor and language delays, and behavioral problems, which were present in both cytogenetic groups. Parental studies demonstrated phenotypically normal carriers in several instances, and mildly affected carriers in others, complicating phenotypic association and/or causality. Possible explanations for these results include reduced penetrance, altered gene dosage on a particular genetic background, or a susceptibility region as reported for other areas of the genome implicated in autism and behavior disturbances.

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  • 10/29 (35%) of individuals with the 15q11.2 BP1-BP2 microdeletion inherited their deletion from an abnormal parent.

    “The review of literature from six published reports summarized by Cafferkey et al. [18] regarding information on the inheritance of the 15q11.2 BP1–BP2 microdeletion indicates that 22/43 (51%) of individuals with the microdeletion, where parental data were available, inherited their deletion from an apparently healthy parent while 10/29 (35%) of individuals inherited their deletion from an abnorma”

    From The 15q11.2 BP1–BP2 Microdeletion Syndrome: A Review (2015) · cites this paper as [13]

    The Results section (‘Parental follow-up studies’; page unavailable) reports that four parents with deletions out of 11 with clinical and family histories had a positive family or self history of features seen in the proband. This supports inheritance from some parents with reported features, but the paper does not report the claimed 10/29 (35%) figure. (LLM, conf=0.85)

    Experimental — accuracy not yet measured

  • 22/43 (51%) of individuals with the 15q11.2 BP1-BP2 microdeletion, where parental data were available, inherited their deletion from an apparently healthy parent.

    “The review of literature from six published reports summarized by Cafferkey et al. [18] regarding information on the inheritance of the 15q11.2 BP1–BP2 microdeletion indicates that 22/43 (51%) of individuals with the microdeletion, where parental data were available, inherited their deletion from an apparently healthy parent while 10/29 (35%) of individuals inherited their deletion from an abnorma”

    From The 15q11.2 BP1–BP2 Microdeletion Syndrome: A Review (2015) · cites this paper as [13]

    The Results (Other; page unavailable) report individuals who inherited a BP1–BP2 deletion from phenotypically normal parents, supporting that such inheritance occurs. The Results (Parental follow-up studies; page unavailable) give different follow-up counts; our copy does not report the claimed 22/43 (51%) figure or establish it for individuals with available parental data. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • The reported de novo deletion frequency ranged from 1/21 (5%) to 2/9 (22%) in subjects reviewed by Cafferkey et al.

    “The reported de novo deletion frequency ranged from 1/21 (5%) [13] to 2/9 (22%) [16] in subjects reviewed by Cafferkey et al. [18].”

    From The 15q11.2 BP1–BP2 Microdeletion Syndrome: A Review (2015) · cites this paper as [13]

    The Results section (‘Parental follow-up studies’; page unavailable) reports one confirmed de novo deletion among 44 individuals with parental follow-up for either a deletion or a duplication. It does not give the claimed denominator of 21 deletion subjects or the resulting 5% frequency; nor does it report the 2/9 endpoint, which the citing sentence assigns to another citation. (LLM, conf=0.83)

    Experimental — accuracy not yet measured

  • A deletion involving the 15q11.2 BP1-BP2 region correlates with language or motor delays, behavioral problems, autism, seizures and occasionally mild dysmorphic features.

    “Collectively, they summarized that a deletion involving this genomic region correlated with language or motor delays, behavioral problems, autism, seizures and occasionally mild dysmorphic features.”

    From The 15q11.2 BP1–BP2 Microdeletion Syndrome: A Review (2015) · cites this paper as [13]

  • Burnside et al. found that 0.86% of approximately 17,000 individuals had an abnormality (deletion or duplication) of the 15q11.2 BP1-BP2 region.

    “They found that 0.86% of the approximate 17,000 individuals had an abnormality (deletion or duplication) of the 15q11.2 BP1–BP2 region.”

    From The 15q11.2 BP1–BP2 Microdeletion Syndrome: A Review (2015) · cites this paper as [13]

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Cited by

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Authors
Burnside, R. D., Pasion, R., Mikhail, F. M., Carroll, A. J., Robin, N. H., Youngs, E. L., Gadi, I. K., Keitges, E., Jaswaney, V. L., Papenhausen, P. R., Potluri, V. R., Risheg, H., Rush, B., Smith, J. L., Schwartz, S., Tepperberg, J. H., & Butler, M. G.
Affiliations
  • LabCorp (United States) (US)
  • University of Alabama at Birmingham (US)
  • University of Kansas (US)
Corresponding author
Burnside, Rachel D.
ORCID
Venue
Human Genetics
Publisher
Springer Science and Business Media LLC
Published
2011-02-27
Volume
130
Issue
4
Pages
517-528
ISSN
  • 0018-7348 (ISSN-L)
  • 0340-6717
  • 1432-1203
DOI
10.1007/s00439-011-0970-4
PMC
PMC6814187
OpenAlex
W2036775611
Cited by
257
References
11
Citations by year
2026: 12 · 2025: 12 · 2024: 9 · 2023: 15 · 2022: 9 · 2021: 20 · 2020: 20 · 2019: 15 · 2018: 14 · 2017: 15 · 2016: 23 · 2015: 30 · 2014: 23 · 2013: 19 · 2012: 15
FWCI
12.37
Type
journal article
Language
en
Open access
Licence
www.springer.com/tdm (tdm)
Locations
  • Human Genetics (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • University of Alabama at Birmingham
  • National Institute of Neurological Disorders and Stroke
  • National Center for Research Resources (U54RR019478)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genomic variations and chromosomal abnormalities
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Syndromes and Imprinting
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
Keywords
segmental duplication, copy number variation, Prader-Willi syndrome, Angelman syndrome, neurodevelopmental delay, language delay, autism spectrum disorder, behavioral problems, seizures, incomplete penetrance, gene dosage
MeSH terms
Adolescent, Adult, Autistic Disorder, Mental Disorders, Child, Developmental Disabilities, Child, Preschool, Chromosome Deletion, Chromosomes, Human, Pair 15, Disease Susceptibility, Female, Humans, Infant, Infant, Newborn, Language Development Disorders, Male, Middle Aged, Speech Disorders, Biomarkers, Angelman Syndrome, In Situ Hybridization, Fluorescence, Oligonucleotide Array Sequence Analysis, Gene Duplication, Gene Expression Profiling, Chromosome Disorders, Adaptor Proteins, Signal Transducing, Comparative Genomic Hybridization, Young Adult

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