Analysis of IFT74 as a candidate gene for chromosome 9p-linked ALS-FTD
A new locus for amyotrophic lateral sclerosis--frontotemporal dementia (ALS-FTD) has recently been ascribed to chromosome 9p. We identified chromosome 9p segregating haplotypes within two families with ALS-FTD (F476 and F2) and undertook mutational screening of candidate genes within this locus. Can...
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| Published in | BMC neurology Vol. 6; no. 1; p. 44 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
BioMed Central Ltd
13.12.2006
BioMed Central BMC |
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| Abstract | A new locus for amyotrophic lateral sclerosis--frontotemporal dementia (ALS-FTD) has recently been ascribed to chromosome 9p.
We identified chromosome 9p segregating haplotypes within two families with ALS-FTD (F476 and F2) and undertook mutational screening of candidate genes within this locus.
Candidate gene sequencing at this locus revealed the presence of a disease segregating stop mutation (Q342X) in the intraflagellar transport 74 (IFT74) gene in family 476 (F476), but no mutation was detected within IFT74 in family 2 (F2). While neither family was sufficiently informative to definitively implicate or exclude IFT74 mutations as a cause of chromosome 9-linked ALS-FTD, the nature of the mutation observed within F476 (predicted to truncate the protein by 258 amino acids) led us to sequence the open reading frame of this gene in a large number of ALS and FTD cases (n = 420). An additional sequence variant (G58D) was found in a case of sporadic semantic dementia. I55L sequence variants were found in three other unrelated affected individuals, but this was also found in a single individual among 800 Human Diversity Gene Panel samples.
Confirmation of the pathogenicity of IFT74 sequence variants will require screening of other chromosome 9p-linked families. |
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| AbstractList | A new locus for amyotrophic lateral sclerosis--frontotemporal dementia (ALS-FTD) has recently been ascribed to chromosome 9p.BACKGROUNDA new locus for amyotrophic lateral sclerosis--frontotemporal dementia (ALS-FTD) has recently been ascribed to chromosome 9p.We identified chromosome 9p segregating haplotypes within two families with ALS-FTD (F476 and F2) and undertook mutational screening of candidate genes within this locus.METHODSWe identified chromosome 9p segregating haplotypes within two families with ALS-FTD (F476 and F2) and undertook mutational screening of candidate genes within this locus.Candidate gene sequencing at this locus revealed the presence of a disease segregating stop mutation (Q342X) in the intraflagellar transport 74 (IFT74) gene in family 476 (F476), but no mutation was detected within IFT74 in family 2 (F2). While neither family was sufficiently informative to definitively implicate or exclude IFT74 mutations as a cause of chromosome 9-linked ALS-FTD, the nature of the mutation observed within F476 (predicted to truncate the protein by 258 amino acids) led us to sequence the open reading frame of this gene in a large number of ALS and FTD cases (n = 420). An additional sequence variant (G58D) was found in a case of sporadic semantic dementia. I55L sequence variants were found in three other unrelated affected individuals, but this was also found in a single individual among 800 Human Diversity Gene Panel samples.RESULTSCandidate gene sequencing at this locus revealed the presence of a disease segregating stop mutation (Q342X) in the intraflagellar transport 74 (IFT74) gene in family 476 (F476), but no mutation was detected within IFT74 in family 2 (F2). While neither family was sufficiently informative to definitively implicate or exclude IFT74 mutations as a cause of chromosome 9-linked ALS-FTD, the nature of the mutation observed within F476 (predicted to truncate the protein by 258 amino acids) led us to sequence the open reading frame of this gene in a large number of ALS and FTD cases (n = 420). An additional sequence variant (G58D) was found in a case of sporadic semantic dementia. I55L sequence variants were found in three other unrelated affected individuals, but this was also found in a single individual among 800 Human Diversity Gene Panel samples.Confirmation of the pathogenicity of IFT74 sequence variants will require screening of other chromosome 9p-linked families.CONCLUSIONConfirmation of the pathogenicity of IFT74 sequence variants will require screening of other chromosome 9p-linked families. Abstract Background A new locus for amyotrophic lateral sclerosis – frontotemporal dementia (ALS-FTD) has recently been ascribed to chromosome 9p. Methods We identified chromosome 9p segregating haplotypes within two families with ALS-FTD (F476 and F2) and undertook mutational screening of candidate genes within this locus. Results Candidate gene sequencing at this locus revealed the presence of a disease segregating stop mutation (Q342X) in the intraflagellar transport 74 (IFT74) gene in family 476 (F476), but no mutation was detected within IFT74 in family 2 (F2). While neither family was sufficiently informative to definitively implicate or exclude IFT74 mutations as a cause of chromosome 9-linked ALS-FTD, the nature of the mutation observed within F476 (predicted to truncate the protein by 258 amino acids) led us to sequence the open reading frame of this gene in a large number of ALS and FTD cases (n = 420). An additional sequence variant (G58D) was found in a case of sporadic semantic dementia. I55L sequence variants were found in three other unrelated affected individuals, but this was also found in a single individual among 800 Human Diversity Gene Panel samples. Conclusion Confirmation of the pathogenicity of IFT74 sequence variants will require screening of other chromosome 9p-linked families. A new locus for amyotrophic lateral sclerosis--frontotemporal dementia (ALS-FTD) has recently been ascribed to chromosome 9p. We identified chromosome 9p segregating haplotypes within two families with ALS-FTD (F476 and F2) and undertook mutational screening of candidate genes within this locus. Candidate gene sequencing at this locus revealed the presence of a disease segregating stop mutation (Q342X) in the intraflagellar transport 74 (IFT74) gene in family 476 (F476), but no mutation was detected within IFT74 in family 2 (F2). While neither family was sufficiently informative to definitively implicate or exclude IFT74 mutations as a cause of chromosome 9-linked ALS-FTD, the nature of the mutation observed within F476 (predicted to truncate the protein by 258 amino acids) led us to sequence the open reading frame of this gene in a large number of ALS and FTD cases (n = 420). An additional sequence variant (G58D) was found in a case of sporadic semantic dementia. I55L sequence variants were found in three other unrelated affected individuals, but this was also found in a single individual among 800 Human Diversity Gene Panel samples. Confirmation of the pathogenicity of IFT74 sequence variants will require screening of other chromosome 9p-linked families. BACKGROUND: A new locus for amyotrophic lateral sclerosis - frontotemporal dementia (ALS-FTD) has recently been ascribed to chromosome 9p. METHODS: We identified chromosome 9p segregating haplotypes within two families with ALS-FTD (F476 and F2) and undertook mutational screening of candidate genes within this locus. RESULTS: Candidate gene sequencing at this locus revealed the presence of a disease segregating stop mutation (Q342X) in the intraflagellar transport 74 (IFT74) gene in family 476 (F476), but no mutation was detected within IFT74 in family 2 (F2). While neither family was sufficiently informative to definitively implicate or exclude IFT74 mutations as a cause of chromosome 9-linked ALS-FTD, the nature of the mutation observed within F476 (predicted to truncate the protein by 258 amino acids) led us to sequence the open reading frame of this gene in a large number of ALS and FTD cases (n = 420). An additional sequence variant (G58D) was found in a case of sporadic semantic dementia. I55L sequence variants were found in three other unrelated affected individuals, but this was also found in a single individual among 800 Human Diversity Gene Panel samples. CONCLUSION: Confirmation of the pathogenicity of IFT74 sequence variants will require screening of other chromosome 9p-linked families. A new locus for amyotrophic lateral sclerosis - frontotemporal dementia (ALS-FTD) has recently been ascribed to chromosome 9p. Methods We identified chromosome 9p segregating haplotypes within two families with ALS-FTD (F476 and F2) and undertook mutational screening of candidate genes within this locus. Results Candidate gene sequencing at this locus revealed the presence of a disease segregating stop mutation (Q342X) in the intraflagellar transport 74 (IFT74) gene in family 476 (F476), but no mutation was detected within IFT74 in family 2 (F2). While neither family was sufficiently informative to definitively implicate or exclude IFT74 mutations as a cause of chromosome 9-linked ALS-FTD, the nature of the mutation observed within F476 (predicted to truncate the protein by 258 amino acids) led us to sequence the open reading frame of this gene in a large number of ALS and FTD cases (n = 420). An additional sequence variant (G58D) was found in a case of sporadic semantic dementia. I55L sequence variants were found in three other unrelated affected individuals, but this was also found in a single individual among 800 Human Diversity Gene Panel samples. Conclusion Confirmation of the pathogenicity of IFT74 sequence variants will require screening of other chromosome 9p-linked families. |
| Author | Pickering-Brown, Stuart Rogaeva, Ekaterina Jain, Shushant Hutton, Michael L Schymick, Jennifer Wassermann, Eric M Singleton, Andrew Momeni, Parastoo Greenway, Matthew J Chiò, Adriano Traynor, Bryan J Huey, Edward D Hardy, John Cookson, Mark R Cairns, Nigel J Rothstein, Jeffrey D Grafman, Jordan Holtzman, David M St George-Hyslop, Peter Berger, Stephen Greggio, Elisa Fung, Hon Chung Adamson, Jennifer Hardiman, Orla |
| AuthorAffiliation | 12 SDGE, National Institute of Mental Health, Bethesda, Maryland, USA 9 Department of Medicine and Physiology, Center for Research in Neurodegenerative Diseases, University of Toronto, Toronto, Canada 2 Department of Neurology, Washington University School of Medicine, St. Louis, Missouri, USA 8 Department of Neuroscience, Mayo Clinic College of Medicine, 4500 San Pablo Road, Jacksonville, Florida, USA 10 Department of Neurology and Neuroscience, Johns Hopkins University, Baltimore, Maryland, USA 4 Department of Clinical Neurological Sciences Royal College of Surgeons in Ireland, Dublin, Ireland 3 Department of Pathology & Immunology, Washington University School of Medicine, St. Louis, Missouri, USA 6 Department of Neuroscience, Via Cherasco 15, 10126 Turin, Italy 1 Laboratory of Neurogenetics, National Institute of Aging, NIH, Bethesda, MD, USA 11 Department of Neurology, Beaumont Hospital, Dublin 9, Ireland 7 Cognitive Neuroscience Section, National Institute of Neurological Diseases and Stro |
| AuthorAffiliation_xml | – name: 7 Cognitive Neuroscience Section, National Institute of Neurological Diseases and Stroke, Bethesda, MD 20892, USA – name: 12 SDGE, National Institute of Mental Health, Bethesda, Maryland, USA – name: 2 Department of Neurology, Washington University School of Medicine, St. Louis, Missouri, USA – name: 11 Department of Neurology, Beaumont Hospital, Dublin 9, Ireland – name: 1 Laboratory of Neurogenetics, National Institute of Aging, NIH, Bethesda, MD, USA – name: 8 Department of Neuroscience, Mayo Clinic College of Medicine, 4500 San Pablo Road, Jacksonville, Florida, USA – name: 10 Department of Neurology and Neuroscience, Johns Hopkins University, Baltimore, Maryland, USA – name: 5 Centre for Clinical Neurosciences, University of Manchester, Greater Manchester Neurosciences Centre, Hope Hospital, Salford, UK – name: 3 Department of Pathology & Immunology, Washington University School of Medicine, St. Louis, Missouri, USA – name: 4 Department of Clinical Neurological Sciences Royal College of Surgeons in Ireland, Dublin, Ireland – name: 6 Department of Neuroscience, Via Cherasco 15, 10126 Turin, Italy – name: 9 Department of Medicine and Physiology, Center for Research in Neurodegenerative Diseases, University of Toronto, Toronto, Canada |
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| Snippet | A new locus for amyotrophic lateral sclerosis--frontotemporal dementia (ALS-FTD) has recently been ascribed to chromosome 9p.
We identified chromosome 9p... A new locus for amyotrophic lateral sclerosis - frontotemporal dementia (ALS-FTD) has recently been ascribed to chromosome 9p. Methods We identified chromosome... A new locus for amyotrophic lateral sclerosis--frontotemporal dementia (ALS-FTD) has recently been ascribed to chromosome 9p.BACKGROUNDA new locus for... BACKGROUND: A new locus for amyotrophic lateral sclerosis - frontotemporal dementia (ALS-FTD) has recently been ascribed to chromosome 9p. METHODS: We... Abstract Background A new locus for amyotrophic lateral sclerosis – frontotemporal dementia (ALS-FTD) has recently been ascribed to chromosome 9p. Methods We... |
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| SubjectTerms | Amyotrophic Lateral Sclerosis - complications Amyotrophic Lateral Sclerosis - epidemiology Amyotrophic Lateral Sclerosis - genetics Base Sequence Chromosome Aberrations - statistics & numerical data Chromosome Mapping Chromosomes, Human, Pair 9 - genetics Dementia - complications Dementia - epidemiology Dementia - genetics Genetic Predisposition to Disease - epidemiology Genetic Predisposition to Disease - genetics Heterozygote Humans Male Middle Aged Molecular Sequence Data Mutation North America Polymorphism, Single Nucleotide - genetics Prevalence Risk Assessment - methods Risk Factors |
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| Title | Analysis of IFT74 as a candidate gene for chromosome 9p-linked ALS-FTD |
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