# 614808

AMYOTROPHIC LATERAL SCLEROSIS 18; ALS18


Phenotype-Gene Relationships

Location Phenotype Phenotype
MIM number
Inheritance Phenotype
mapping key
Gene/Locus Gene/Locus
MIM number
17p13.2 Amyotrophic lateral sclerosis 18 614808 3 PFN1 176610
Phenotypic Series

Amyotrophic lateral sclerosis - PS105400 - 32 Entries
Location Phenotype Inheritance Phenotype
mapping key
Phenotype
MIM number
Gene/Locus Gene/Locus
MIM number
1p36.22 Frontotemporal lobar degeneration, TARDBP-related AD 3 612069 TARDBP 605078
1p36.22 Amyotrophic lateral sclerosis 10, with or without FTD AD 3 612069 TARDBP 605078
2p13.1 {Amyotrophic lateral sclerosis, susceptibility to} AR, AD 3 105400 DCTN1 601143
2q33.1 Amyotrophic lateral sclerosis 2, juvenile AR 3 205100 ALS2 606352
2q34 Amyotrophic lateral sclerosis 19 AD 3 615515 ERBB4 600543
2q35 Amyotrophic lateral sclerosis 22 with or without frontotemoral dementia AD 3 616208 TUBA4A 191110
3p11.2 Amyotrophic lateral sclerosis 17 AD 3 614696 CHMP2B 609512
5q31.2 Amyotrophic lateral sclerosis 21 AD 3 606070 MATR3 164015
5q35.3 Frontotemporal dementia and/or amyotrophic lateral sclerosis 3 AD 3 616437 SQSTM1 601530
6q21 Amyotrophic lateral sclerosis 11 AD 3 612577 FIG4 609390
9p21.2 Frontotemporal dementia and/or amyotrophic lateral sclerosis 1 AD 3 105550 C9orf72 614260
9p13.3 ?Amyotrophic lateral sclerosis 16, juvenile AR 3 614373 SIGMAR1 601978
9p13.3 Amyotrophic lateral sclerosis 14, with or without frontotemporal dementia 3 613954 VCP 601023
9q34.13 Amyotrophic lateral sclerosis 4, juvenile AD 3 602433 SETX 608465
10p13 Amyotrophic lateral sclerosis 12 3 613435 OPTN 602432
12q13.12 {Amyotrophic lateral sclerosis, susceptibility to} AR, AD 3 105400 PRPH 170710
12q13.13 Amyotrophic lateral sclerosis 20 AD 3 615426 HNRNPA1 164017
12q14.2 Frontotemporal dementia and/or amyotrophic lateral sclerosis 4 AD 3 616439 TBK1 604834
12q24.12 Spinocerebellar ataxia 2 AD 3 183090 ATXN2 601517
12q24.12 {Amyotrophic lateral sclerosis, susceptibility to, 13} AD 3 183090 ATXN2 601517
14q11.2 Amyotrophic lateral sclerosis 9 3 611895 ANG 105850
15q21.1 Amyotrophic lateral sclerosis 5, juvenile AR 3 602099 SPG11 610844
16p11.2 Amyotrophic lateral sclerosis 6, with or without frontotemporal dementia 3 608030 FUS 137070
17p13.2 Amyotrophic lateral sclerosis 18 3 614808 PFN1 176610
18q21 Amyotrophic lateral sclerosis 3 AD 2 606640 ALS3 606640
20p13 Amyotrophic lateral sclerosis 7 2 608031 ALS7 608031
20q13.32 Amyotrophic lateral sclerosis 8 AD 3 608627 VAPB 605704
21q22.11 Amyotrophic lateral sclerosis 1 AR, AD 3 105400 SOD1 147450
22q11.23 Frontotemporal dementia and/or amyotrophic lateral sclerosis 2 AD 3 615911 CHCHD10 615903
22q12.2 ?{Amyotrophic lateral sclerosis, susceptibility to} AR, AD 3 105400 NEFH 162230
Xp11.21 Amyotrophic lateral sclerosis 15, with or without frontotemporal dementia XLD 3 300857 UBQLN2 300264
Not Mapped Amyotrophic lateral sclerosis, juvenile, with dementia 205200 ALSDC 205200

TEXT

A number sign (#) is used with this entry because amyotrophic lateral sclerosis-18 (ALS18) is caused by heterozygous mutation in the PFN1 gene (176610) on chromosome 17p.

For a phenotypic description and a discussion of genetic heterogeneity of amyotrophic lateral sclerosis (ALS), see ALS1 (105400).


Clinical Features

Among 22 cases of ALS that resulted from mutations in PFN1 (ALS18), all displayed limb onset. Given that bulbar onset represents approximately 25% of ALS cases, Wu et al. (2012) proposed that their observation suggests a common clinical phenotype among patients with PFN1 mutations. The age of onset for familial ALS18 cases was 44.8 +/- 7.4 years.


Mapping

Wu et al. (2012) performed exome capture followed by deep sequencing on 2 large ALS families of Caucasian (family 1) and Sephardic Jewish (family 2) origin. Both displayed a dominant inheritance mode and were negative for known ALS-causing mutations. For each family, 2 affected members with maximum genetic distance were selected for exome sequencing. More than 150X coverage was achieved. Using a variety of filters, Wu et al. (2012) were able to reduce the number of candidate mutations to 2 within family 1 and 3 within family 2.


Molecular Genetics

Wu et al. (2012) identified 4 different missense mutations in 7 families segregating autosomal dominant ALS. Sequencing of the PFN coding region in 816 sporadic ALS samples identified 2 samples containing the E117G mutation (176610.0004). In each of the mutations, the altered amino acid was evolutionarily conserved down to the level of zebrafish.


REFERENCES

  1. Wu, C.-H., Fallini, C., Ticozzi, N., Keagle, P. J., Sapp, P. C., Piotrowska, K., Lowe, P., Koppers, M., McKenna-Yasek, D., Baron, D. M., Kost, J. E., Gonzalez-Perez, P., and 26 others. Mutations in the profilin 1 gene cause familial amyotrophic lateral sclerosis. Nature 488: 499-503, 2012. [PubMed: 22801503, images, related citations] [Full Text]


Creation Date:
Ada Hamosh : 9/5/2012
Edit History:
alopez : 09/06/2012

# 614808

AMYOTROPHIC LATERAL SCLEROSIS 18; ALS18


ORPHA: 803;   DO: 0060209;  


Phenotype-Gene Relationships

Location Phenotype Phenotype
MIM number
Inheritance Phenotype
mapping key
Gene/Locus Gene/Locus
MIM number
17p13.2 Amyotrophic lateral sclerosis 18 614808 3 PFN1 176610

TEXT

A number sign (#) is used with this entry because amyotrophic lateral sclerosis-18 (ALS18) is caused by heterozygous mutation in the PFN1 gene (176610) on chromosome 17p.

For a phenotypic description and a discussion of genetic heterogeneity of amyotrophic lateral sclerosis (ALS), see ALS1 (105400).


Clinical Features

Among 22 cases of ALS that resulted from mutations in PFN1 (ALS18), all displayed limb onset. Given that bulbar onset represents approximately 25% of ALS cases, Wu et al. (2012) proposed that their observation suggests a common clinical phenotype among patients with PFN1 mutations. The age of onset for familial ALS18 cases was 44.8 +/- 7.4 years.


Mapping

Wu et al. (2012) performed exome capture followed by deep sequencing on 2 large ALS families of Caucasian (family 1) and Sephardic Jewish (family 2) origin. Both displayed a dominant inheritance mode and were negative for known ALS-causing mutations. For each family, 2 affected members with maximum genetic distance were selected for exome sequencing. More than 150X coverage was achieved. Using a variety of filters, Wu et al. (2012) were able to reduce the number of candidate mutations to 2 within family 1 and 3 within family 2.


Molecular Genetics

Wu et al. (2012) identified 4 different missense mutations in 7 families segregating autosomal dominant ALS. Sequencing of the PFN coding region in 816 sporadic ALS samples identified 2 samples containing the E117G mutation (176610.0004). In each of the mutations, the altered amino acid was evolutionarily conserved down to the level of zebrafish.


REFERENCES

  1. Wu, C.-H., Fallini, C., Ticozzi, N., Keagle, P. J., Sapp, P. C., Piotrowska, K., Lowe, P., Koppers, M., McKenna-Yasek, D., Baron, D. M., Kost, J. E., Gonzalez-Perez, P., and 26 others. Mutations in the profilin 1 gene cause familial amyotrophic lateral sclerosis. Nature 488: 499-503, 2012. [PubMed: 22801503] [Full Text: https://dx.doi.org/10.1038/nature11280]


Creation Date:
Ada Hamosh : 9/5/2012
Edit History:
alopez : 09/06/2012