Importance of Genetic Studies in Consanguineous Populations for the Characterization of Novel Human Gene Functions

Summary Consanguineous offspring have elevated levels of homozygosity. Autozygous stretches within their genome are likely to harbour loss of function (LoF) mutations which will lead to complete inactivation or dysfunction of genes. Studying consanguineous offspring with clinical phenotypes has been...

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Vydané v:Annals of human genetics Ročník 80; číslo 3; s. 187 - 196
Hlavní autori: Erzurumluoglu, A. Mesut, Shihab, Hashem A., Rodriguez, Santiago, Gaunt, Tom R., Day, Ian N.M.
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: England Wiley Subscription Services, Inc 01.05.2016
John Wiley and Sons Inc
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ISSN:0003-4800, 1469-1809, 1469-1809
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Abstract Summary Consanguineous offspring have elevated levels of homozygosity. Autozygous stretches within their genome are likely to harbour loss of function (LoF) mutations which will lead to complete inactivation or dysfunction of genes. Studying consanguineous offspring with clinical phenotypes has been very useful for identifying disease causal mutations. However, at present, most of the genes in the human genome have no disorder associated with them or have unknown function. This is presumably mostly due to the fact that homozygous LoF variants are not observed in outbred populations which are the main focus of large sequencing projects. However, another reason may be that many genes in the genome—even when completely “knocked out,” do not cause a distinct or defined phenotype. Here, we discuss the benefits and implications of studying consanguineous populations, as opposed to the traditional approach of analysing a subset of consanguineous families or individuals with disease. We suggest that studying consanguineous populations “as a whole” can speed up the characterisation of novel gene functions as well as indicating nonessential genes and/or regions in the human genome. We also suggest designing a single nucleotide variant (SNV) array to make the process more efficient.
AbstractList Summary Consanguineous offspring have elevated levels of homozygosity. Autozygous stretches within their genome are likely to harbour loss of function (LoF) mutations which will lead to complete inactivation or dysfunction of genes. Studying consanguineous offspring with clinical phenotypes has been very useful for identifying disease causal mutations. However, at present, most of the genes in the human genome have no disorder associated with them or have unknown function. This is presumably mostly due to the fact that homozygous LoF variants are not observed in outbred populations which are the main focus of large sequencing projects. However, another reason may be that many genes in the genome—even when completely “knocked out,” do not cause a distinct or defined phenotype. Here, we discuss the benefits and implications of studying consanguineous populations, as opposed to the traditional approach of analysing a subset of consanguineous families or individuals with disease. We suggest that studying consanguineous populations “as a whole” can speed up the characterisation of novel gene functions as well as indicating nonessential genes and/or regions in the human genome. We also suggest designing a single nucleotide variant (SNV) array to make the process more efficient.
Consanguineous offspring have elevated levels of homozygosity. Autozygous stretches within their genome are likely to harbour loss of function (LoF) mutations which will lead to complete inactivation or dysfunction of genes. Studying consanguineous offspring with clinical phenotypes has been very useful for identifying disease causal mutations. However, at present, most of the genes in the human genome have no disorder associated with them or have unknown function. This is presumably mostly due to the fact that homozygous LoF variants are not observed in outbred populations which are the main focus of large sequencing projects. However, another reason may be that many genes in the genome—even when completely “knocked out,” do not cause a distinct or defined phenotype. Here, we discuss the benefits and implications of studying consanguineous populations, as opposed to the traditional approach of analysing a subset of consanguineous families or individuals with disease. We suggest that studying consanguineous populations “as a whole” can speed up the characterisation of novel gene functions as well as indicating nonessential genes and/or regions in the human genome. We also suggest designing a single nucleotide variant (SNV) array to make the process more efficient.
Summary Consanguineous offspring have elevated levels of homozygosity. Autozygous stretches within their genome are likely to harbour loss of function (LoF) mutations which will lead to complete inactivation or dysfunction of genes. Studying consanguineous offspring with clinical phenotypes has been very useful for identifying disease causal mutations. However, at present, most of the genes in the human genome have no disorder associated with them or have unknown function. This is presumably mostly due to the fact that homozygous LoF variants are not observed in outbred populations which are the main focus of large sequencing projects. However, another reason may be that many genes in the genome--even when completely "knocked out," do not cause a distinct or defined phenotype. Here, we discuss the benefits and implications of studying consanguineous populations, as opposed to the traditional approach of analysing a subset of consanguineous families or individuals with disease. We suggest that studying consanguineous populations "as a whole" can speed up the characterisation of novel gene functions as well as indicating nonessential genes and/or regions in the human genome. We also suggest designing a single nucleotide variant (SNV) array to make the process more efficient.
Consanguineous offspring have elevated levels of homozygosity. Autozygous stretches within their genome are likely to harbour loss of function (LoF) mutations which will lead to complete inactivation or dysfunction of genes. Studying consanguineous offspring with clinical phenotypes has been very useful for identifying disease causal mutations. However, at present, most of the genes in the human genome have no disorder associated with them or have unknown function. This is presumably mostly due to the fact that homozygous LoF variants are not observed in outbred populations which are the main focus of large sequencing projects. However, another reason may be that many genes in the genome-even when completely "knocked out," do not cause a distinct or defined phenotype. Here, we discuss the benefits and implications of studying consanguineous populations, as opposed to the traditional approach of analysing a subset of consanguineous families or individuals with disease. We suggest that studying consanguineous populations "as a whole" can speed up the characterisation of novel gene functions as well as indicating nonessential genes and/or regions in the human genome. We also suggest designing a single nucleotide variant (SNV) array to make the process more efficient.Consanguineous offspring have elevated levels of homozygosity. Autozygous stretches within their genome are likely to harbour loss of function (LoF) mutations which will lead to complete inactivation or dysfunction of genes. Studying consanguineous offspring with clinical phenotypes has been very useful for identifying disease causal mutations. However, at present, most of the genes in the human genome have no disorder associated with them or have unknown function. This is presumably mostly due to the fact that homozygous LoF variants are not observed in outbred populations which are the main focus of large sequencing projects. However, another reason may be that many genes in the genome-even when completely "knocked out," do not cause a distinct or defined phenotype. Here, we discuss the benefits and implications of studying consanguineous populations, as opposed to the traditional approach of analysing a subset of consanguineous families or individuals with disease. We suggest that studying consanguineous populations "as a whole" can speed up the characterisation of novel gene functions as well as indicating nonessential genes and/or regions in the human genome. We also suggest designing a single nucleotide variant (SNV) array to make the process more efficient.
Author Rodriguez, Santiago
Gaunt, Tom R.
Day, Ian N.M.
Erzurumluoglu, A. Mesut
Shihab, Hashem A.
AuthorAffiliation 2 MRC Integrative Epidemiology Unit (IEU), School of Social and Community Medicine University of Bristol Bristol UK
1 Bristol Genetic Epidemiology Laboratories (BGEL), School of Social and Community Medicine University of Bristol Bristol UK
3 Genetic Epidemiology Group, Department of Health Sciences University of Leicester Leicester UK
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Cites_doi 10.1093/hmg/ddq365
10.1038/nmeth0410-248
10.1073/pnas.0906079106
10.1038/nrg3118
10.1038/sj.ejhg.5201649
10.1375/twin.11.3.249
10.1002/humu.22220
10.1038/gim.2011.28
10.1007/978-1-4020-2231-9
10.1126/science.1215040
10.1371/journal.pone.0121351
10.1017/S0021932003005911
10.1002/mgg3.97
10.1093/bioinformatics/btv009
10.1038/nature08250
10.1017/S0021932012000016
10.1007/s00439-002-0877-1
10.1016/S0140-6736(13)61132-0
10.1080/02724936.1997.11747879
10.1038/43185
10.1371/journal.pgen.1004030
10.1002/humu.22376
10.1093/nar/gkg509
10.1017/S0021932000006660
10.1017/CBO9781139015844
10.1155/2015/923491
10.1525/as.2009.49.1.16
10.1073/pnas.94.10.5189
10.1017/S0021932097004914
10.1097/GIM.0b013e318217477f
10.1073/pnas.0709013104
10.1093/genetics/163.3.1011
10.1111/j.1469-1809.1994.tb00729.x
10.1038/ng.2892
10.1002/humu.22225
10.1038/nrg3053
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Issue 3
Keywords complex disease
gene function
Consanguineous populations
Mendelian disease
autozygosity
Language English
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2016 The Authors. Annals of Human Genetics published by University College London (UCL) and John Wiley & Sons Ltd.
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References 2007; 104
2012
2010; 107
2010; 19
1997; 47
2006; 14
2003; 35
1997; 29
2014; 46
2011; 13
2004
2008; 11
2013; 382
2011; 12
2012; 14
2003; 112
2009; 49
2003; 31
2013; 9
2007; 28
1997; 94
2014; 2
2001
2015a
2013; 34
1997; 387
1997; 17
1994; 58
2015
2013
2009; 461
1988; 20
2012; 335
2012; 44
2010; 7
2015b; 10
2003; 163
e_1_2_5_27_1
e_1_2_5_28_1
Chandrasekhara Rao R. V. R. (e_1_2_5_11_1) 2013
e_1_2_5_25_1
e_1_2_5_26_1
e_1_2_5_23_1
e_1_2_5_24_1
e_1_2_5_45_1
e_1_2_5_21_1
e_1_2_5_44_1
e_1_2_5_43_1
Saleheen D. (e_1_2_5_39_1) 2015
e_1_2_5_29_1
Rudan I. (e_1_2_5_37_1) 2003; 163
e_1_2_5_42_1
e_1_2_5_20_1
e_1_2_5_41_1
e_1_2_5_40_1
Kim T. J. (e_1_2_5_22_1) 2013
e_1_2_5_15_1
Narasimhan V. (e_1_2_5_31_1) 2015
e_1_2_5_38_1
e_1_2_5_14_1
e_1_2_5_17_1
e_1_2_5_36_1
e_1_2_5_9_1
e_1_2_5_16_1
Hashmi M. A. (e_1_2_5_18_1) 1997; 47
e_1_2_5_8_1
e_1_2_5_34_1
e_1_2_5_7_1
e_1_2_5_10_1
e_1_2_5_35_1
e_1_2_5_6_1
e_1_2_5_32_1
e_1_2_5_5_1
e_1_2_5_12_1
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e_1_2_5_4_1
e_1_2_5_3_1
e_1_2_5_2_1
e_1_2_5_19_1
El‐Mouzan M. I. (e_1_2_5_13_1) 2007; 28
e_1_2_5_30_1
References_xml – volume: 58
  start-page: 321
  year: 1994
  end-page: 329
  article-title: Consanguineous marriage in Turkey and its impact on fertility and mortality
  publication-title: Ann Hum Genet
– volume: 9
  start-page: e1004030
  year: 2013
  article-title: Autozygome sequencing expands the horizon of human knockout research and provides novel insights into human phenotypic variation
  publication-title: PLoS Genet
– volume: 10
  start-page: e0121351
  issue: 3
  year: 2015b
  article-title: Proxy Molecular Diagnosis from Whole‐Exome Sequencing Reveals Papillon‐Lefevre Syndrome Caused by a Missense Mutation in CTSC
  publication-title: PLoS ONE
– volume: 46
  start-page: 310
  year: 2014
  end-page: 315
  publication-title: Nat Genet
– volume: 17
  start-page: 155
  year: 1997
  end-page: 160
  article-title: Consanguineous marriages in a Saudi population and the effect of inbreeding on prenatal and postnatal mortality
  publication-title: Ann Trop Paediatr
– volume: 20
  start-page: 333
  year: 1988
  end-page: 336
  article-title: Inbreeding levels in Khartoum
  publication-title: J Biosoc Sci
– year: 2001
– year: 2015
  article-title: Health and population effects of rare gene knockouts in adult humans with related parents
  publication-title: bioRxiv
– volume: 44
  start-page: 571
  year: 2012
  end-page: 594
  article-title: The practice of consanguineous marriage in Oman: Prevalence, trends and determinants
  publication-title: J Biosoc Sci
– volume: 31
  start-page: 3812
  year: 2003
  end-page: 3814
  article-title: SIFT: Predicting amino acid changes that affect protein function
  publication-title: Nucleic Acids Res
– volume: 382
  start-page: 1350
  year: 2013
  end-page: 1359
  article-title: Risk factors for congenital anomaly in a multiethnic birth cohort: An analysis of the Born in Bradford study
  publication-title: Lancet
– volume: 7
  start-page: 248
  year: 2010
  end-page: 249
  article-title: A method and server for predicting damaging missense mutations
  publication-title: Nat Methods
– volume: 12
  start-page: 692
  year: 2011
  end-page: 702
  article-title: The evolutionary origin of orphan genes
  publication-title: Nature Rev Genet
– volume: 2
  start-page: 369
  year: 2014
  end-page: 378
  article-title: Genetics and genomic medicine in Saudi Arabia
  publication-title: Mol Genet Genomic Med
– volume: 94
  start-page: 5189
  year: 1997
  end-page: 5194
  article-title: An essential cell division gene of Drosophila, absent from Saccharomyces, encodes an unusual protein with tubulin‐like and myosin‐like peptide motifs
  publication-title: Proc Natl Acad Sci U S A
– volume: 49
  start-page: 16
  year: 2009
  end-page: 27
  article-title: Pakistan in 2008: Moving beyond Musharraf
  publication-title: Asian Survey
– volume: 34
  start-page: 57
  year: 2013
  end-page: 65
  article-title: Predicting the functional, molecular, and phenotypic consequences of amino acid substitutions using hidden Markov models
  publication-title: Hum Mutat
– year: 2015
  article-title: Human knockouts in a cohort with a high rate of consanguinity
  publication-title: bioRxiv
– volume: 461
  start-page: 272
  year: 2009
  end-page: 276
  article-title: Targeted capture and massively parallel sequencing of 12 human exomes
  publication-title: Nature
– year: 2012
– volume: 104
  start-page: 19428
  year: 2007
  end-page: 19433
  article-title: Distinguishing protein‐coding and noncoding genes in the human genome
  publication-title: Proc Natl Acad Sci U S A
– volume: 14
  start-page: 515
  year: 2012
  end-page: 519
  article-title: Autozygome maps dispensable DNA and reveals potential selective bias against nullizygosity
  publication-title: Genet Med
– volume: 163
  start-page: 1011
  year: 2003
  end-page: 1021
  article-title: Inbreeding and the genetic complexity of human hypertension
  publication-title: Genetics
– volume: 387
  start-page: 903
  year: 1997
  end-page: 908
  article-title: Congenital leptin deficiency is associated with severe early‐onset obesity in humans
  publication-title: Nature
– volume: 19
  start-page: R125
  year: 2010
  end-page: R130
  article-title: Loss‐of‐function variants in the genomes of healthy humans
  publication-title: Hum Mol Genet
– start-page: 1536
  year: 2015
  end-page: 1543
  article-title: An integrative approach to predicting the functional effects of non‐coding and coding sequence variation
  publication-title: Bioinformatics
– volume: 29
  start-page: 491
  year: 1997
  end-page: 497
  article-title: Consanguineous marriages in the United Arab Emirates
  publication-title: J Biosoc Sci
– volume: 34
  start-page: E2393
  year: 2013
  end-page: E2402
  article-title: dbNSFP v2.0: A database of human non‐synonymous SNVs and their functional predictions and annotations
  publication-title: Hum Mutat
– year: 2004
– volume: 28
  start-page: 1881
  year: 2007
  end-page: 1884
  article-title: Regional variations in the prevalence of consanguinity in Saudi Arabia
  publication-title: Saudi Med J
– year: 2015a
  article-title: Identifying highly‐penetrant disease causal mutations using next generation sequencing: Guide to whole process
  publication-title: Biomed Res Int
– volume: 13
  start-page: 135
  year: 2011
  end-page: 145
  article-title: Rare and common variants: Twenty arguments
  publication-title: Nat Rev Genet
– volume: 47
  start-page: 75
  year: 1997
  end-page: 78
  article-title: Frequency of consanguinity and its effect on congenital malformation—A hospital based study
  publication-title: JPMA
– volume: 112
  start-page: 470
  year: 2003
  end-page: 526
  article-title: The Finnish Disease Heritage III: The individual diseases
  publication-title: Hum Genet
– volume: 35
  start-page: 513
  year: 2003
  end-page: 526
  article-title: Effects of polygyny and consanguinity on high fertility in the rural Arab population in South Jordan
  publication-title: J Biosoc Sci
– volume: 14
  start-page: 1074
  year: 2006
  end-page: 1081
  article-title: Nonsense‐mediated mRNA decay modulates clinical outcome of genetic disease
  publication-title: Eur J Hum Genet
– volume: 34
  start-page: 50
  year: 2013
  end-page: 56
  article-title: Autozygosity mapping with exome sequence data
  publication-title: Hum Mutat
– volume: 13
  start-page: 841
  year: 2011
  end-page: 847
  article-title: Consanguineous marriages, pearls and perils: Geneva International Consanguinity Workshop Report
  publication-title: Genet Med
– volume: 335
  start-page: 823
  year: 2012
  end-page: 828
  article-title: A systematic survey of loss‐of‐function variants in human protein‐coding genes
  publication-title: Science
– volume: 107
  start-page: 1779
  year: 2010
  end-page: 1786
  article-title: Consanguinity, human evolution, and complex diseases
  publication-title: Proc Natl Acad Sci U S A
– volume: 11
  start-page: 249
  year: 2008
  end-page: 256
  article-title: A century of Hardy‐Weinberg equilibrium
  publication-title: Twin Res Hum Genet
– year: 2013
– year: 2015
  ident: e_1_2_5_31_1
  article-title: Health and population effects of rare gene knockouts in adult humans with related parents
  publication-title: bioRxiv
– ident: e_1_2_5_27_1
  doi: 10.1093/hmg/ddq365
– ident: e_1_2_5_2_1
  doi: 10.1038/nmeth0410-248
– ident: e_1_2_5_9_1
  doi: 10.1073/pnas.0906079106
– ident: e_1_2_5_16_1
  doi: 10.1038/nrg3118
– volume-title: Encyclopædia Britannica
  year: 2013
  ident: e_1_2_5_11_1
– ident: e_1_2_5_20_1
  doi: 10.1038/sj.ejhg.5201649
– ident: e_1_2_5_28_1
  doi: 10.1375/twin.11.3.249
– ident: e_1_2_5_10_1
  doi: 10.1002/humu.22220
– ident: e_1_2_5_21_1
  doi: 10.1038/gim.2011.28
– ident: e_1_2_5_24_1
  doi: 10.1007/978-1-4020-2231-9
– ident: e_1_2_5_26_1
  doi: 10.1126/science.1215040
– ident: e_1_2_5_15_1
  doi: 10.1371/journal.pone.0121351
– volume: 28
  start-page: 1881
  year: 2007
  ident: e_1_2_5_13_1
  article-title: Regional variations in the prevalence of consanguinity in Saudi Arabia
  publication-title: Saudi Med J
– ident: e_1_2_5_7_1
– volume: 47
  start-page: 75
  year: 1997
  ident: e_1_2_5_18_1
  article-title: Frequency of consanguinity and its effect on congenital malformation—A hospital based study
  publication-title: JPMA
– ident: e_1_2_5_43_1
  doi: 10.1017/S0021932003005911
– ident: e_1_2_5_5_1
  doi: 10.1002/mgg3.97
– ident: e_1_2_5_42_1
  doi: 10.1093/bioinformatics/btv009
– year: 2015
  ident: e_1_2_5_39_1
  article-title: Human knockouts in a cohort with a high rate of consanguinity
  publication-title: bioRxiv
– ident: e_1_2_5_36_1
– ident: e_1_2_5_34_1
  doi: 10.1038/nature08250
– ident: e_1_2_5_19_1
  doi: 10.1017/S0021932012000016
– ident: e_1_2_5_35_1
  doi: 10.1007/s00439-002-0877-1
– ident: e_1_2_5_40_1
  doi: 10.1016/S0140-6736(13)61132-0
– ident: e_1_2_5_4_1
  doi: 10.1080/02724936.1997.11747879
– ident: e_1_2_5_30_1
  doi: 10.1038/43185
– ident: e_1_2_5_6_1
  doi: 10.1371/journal.pgen.1004030
– ident: e_1_2_5_25_1
  doi: 10.1002/humu.22376
– ident: e_1_2_5_33_1
  doi: 10.1093/nar/gkg509
– ident: e_1_2_5_38_1
  doi: 10.1017/S0021932000006660
– ident: e_1_2_5_8_1
  doi: 10.1017/CBO9781139015844
– ident: e_1_2_5_14_1
  doi: 10.1155/2015/923491
– ident: e_1_2_5_32_1
  doi: 10.1525/as.2009.49.1.16
– ident: e_1_2_5_29_1
  doi: 10.1073/pnas.94.10.5189
– ident: e_1_2_5_3_1
  doi: 10.1017/S0021932097004914
– ident: e_1_2_5_17_1
  doi: 10.1097/GIM.0b013e318217477f
– ident: e_1_2_5_12_1
  doi: 10.1073/pnas.0709013104
– volume: 163
  start-page: 1011
  year: 2003
  ident: e_1_2_5_37_1
  article-title: Inbreeding and the genetic complexity of human hypertension
  publication-title: Genetics
  doi: 10.1093/genetics/163.3.1011
– ident: e_1_2_5_45_1
  doi: 10.1111/j.1469-1809.1994.tb00729.x
– ident: e_1_2_5_23_1
  doi: 10.1038/ng.2892
– ident: e_1_2_5_41_1
  doi: 10.1002/humu.22225
– ident: e_1_2_5_44_1
  doi: 10.1038/nrg3053
– volume-title: Encyclopædia Britannica
  year: 2013
  ident: e_1_2_5_22_1
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Snippet Summary Consanguineous offspring have elevated levels of homozygosity. Autozygous stretches within their genome are likely to harbour loss of function (LoF)...
Consanguineous offspring have elevated levels of homozygosity. Autozygous stretches within their genome are likely to harbour loss of function (LoF) mutations...
Summary Consanguineous offspring have elevated levels of homozygosity. Autozygous stretches within their genome are likely to harbour loss of function (LoF)...
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pubmed
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wiley
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SubjectTerms autozygosity
Chromosome Mapping
complex disease
Consanguineous populations
Consanguinity
gene function
Gene Silencing
Genes
Genetics, Population
Genome, Human
Genomes
Heterozygote
Homozygote
Humans
Mendelian disease
Mutation
Phenotype
Review
Title Importance of Genetic Studies in Consanguineous Populations for the Characterization of Novel Human Gene Functions
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fahg.12150
https://www.ncbi.nlm.nih.gov/pubmed/27000383
https://www.proquest.com/docview/1781665236
https://www.proquest.com/docview/1782834630
https://www.proquest.com/docview/1787968889
https://pubmed.ncbi.nlm.nih.gov/PMC4949565
Volume 80
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