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1. Structural mapping of GABRB3 variants reveals genotype–phenotype correlations

Author

Johannesen, Katrine M., Iqbal, Sumaiya, Guazzi, Milena, Mohammadi, Nazanin A., Pérez-Palma, Eduardo, Schaefer, Elise, De Saint Martin, Anne, Abiwarde, Marie Therese, McTague, Amy, Pons, Roser, Piton, Amelie, Kurian, Manju A., Ambegaonkar, Gautam, Firth, Helen, Sanchis-Juan, Alba, Deprez, Marie, Jansen, Katrien, De Waele, Liesbeth, Briltra, Eva H., Verbeek, Nienke E., van Kempen, Marjan, Fazeli, Walid, Striano, Pasquale, Zara, Federico, Visser, Gerhard, Braakman, Hilde M.H., Haeusler, Martin, Elbracht, Miriam, Vaher, Ulvi, Smol, Thomas, Lemke, Johannes R., Platzer, Konrad, Kennedy, Joanna, Klein, Karl Martin, Au, Ping Yee Billie, Smyth, Kimberly, Kaplan, Julie, Thomas, Morgan, Dewenter, Malin K., Dinopoulos, Argirios, Campbell, Arthur J., Lal, Dennis, Lederer, Damien, Liao, Vivian W.Y., Ahring, Philip K., Møller, Rikke S., and Gardella, Elena

Published
2022
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2. Acral lamellar ichthyosis with amino acid substitution in the C‐terminus of keratin 2

Author

Leonie Frommherz, Katalin Komlosi, Charlotte Hewel, Julia Kopp, Malin Dewenter, Andreas Zimmer, Oliver Bartsch, Matthias Linke, Kristin Technau‐Hafsi, Susanne Gerber, Judith Fischer, and Cristina Has

Subjects
Infectious Diseases, Dermatology
Abstract

Most cases of hereditary ichthyoses present with generalized scaling and skin dryness. However, in some cases skin involvement is restricted to particular body regions as in acral lamellar ichthyosis.We report on the genetic basis of acral ichthyosis in two families presenting with a similar phenotype.Genetic testing was performed by targeted next generation sequencing and whole-exome sequencing. For identity-by-descent analysis, the parents were genotyped and data analysis was performed with the Chromosome Analysis Suite Software. RT-PCR with RNA extracted from skin samples was used to analyse the effect of variants on splicing.Genetic testing identified a few heterozygous variants, but only the variant in KRT2 c.1912 T C, p.Phe638Leu segregated with the disease and remained the strongest candidate. Pairwise identity-by-descent analysis revealed no indication of family relationship. Phenylalanine 638 is the second last amino acid upstream of the termination codon in the tail of K2, and substitution to leucine is predicted as probably damaging. Assessment of the variant is difficult, in part due to the lack of crystal structures of this region.Altogether, we show that a type of autosomal dominant acral ichthyosis is most probably caused by an amino acid substitution in the C-terminus of keratin 2.

Published
2022
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3. Assessment of the Genetic Spectrum of Uncombable Hair Syndrome in a Cohort of 107 Individuals

Author

F. Buket Basmanav, Nicole Cesarato, Sheetal Kumar, Oleg Borisov, Pavlos Kokordelis, Damian J. Ralser, Maria Wehner, Daisy Axt, Xing Xiong, Holger Thiele, Vadim Dolgin, Yasmina Gossmann, Nadine Fricker, Malin Katharina Dewenter, Karsten Weller, Mohnish Suri, Herbert Reichenbach, Vinzenz Oji, Marie-Claude Addor, Karla Ramirez, Helen Stewart, Natalie Garcia Bartels, Lisa Weibel, Nicola Wagner, Susannah George, Arzu Kilic, Iliana Tantcheva-Poor, Alison Stewart, Nicola Dikow, Bettina Blaumeiser, Márta Medvecz, Ulrike Blume-Peytavi, Paul Farrant, Ramon Grimalt, Sara Bertok, Lisa Bradley, Marina Eskin-Schwartz, Ohad Samuel Birk, Anette Bygum, Michel Simon, Peter Krawitz, Christine Fischer, Henning Hamm, Günter Fritz, and Regina C. Betz

Subjects
Male, Cohort Studies, Transglutaminases, Exome Sequencing, Humans, Female, Human medicine, Dermatology, Hair Diseases, Hair
Abstract

ImportanceUncombable hair syndrome (UHS) is a rare hair shaft anomaly that manifests during infancy and is characterized by dry, frizzy, and wiry hair that cannot be combed flat. Only about 100 known cases have been reported so far.ObjectiveTo elucidate the genetic spectrum of UHS.Design, Setting, and ParticipantsThis cohort study includes 107 unrelated index patients with a suspected diagnosis of UHS and family members who were recruited worldwide from January 2013 to December 2021. Participants of all ages, races, and ethnicities were recruited at referral centers or were enrolled on their own initiative following personal contact with the authors. Genetic analyses were conducted in Germany from January 2014 to December 2021.Main Outcomes and MeasuresClinical photographs, Sanger or whole-exome sequencing and array-based genotyping of DNA extracted from blood or saliva samples, and 3-dimensional protein modeling. Descriptive statistics, such as frequency counts, were used to describe the distribution of identified pathogenic variants and genotypes.ResultsThe genetic characteristics of patients with UHS were established in 80 of 107 (74.8%) index patients (82 [76.6%] female) who carried biallelic pathogenic variants in PADI3, TGM3, or TCHH (ie, genes that encode functionally related hair shaft proteins). Molecular genetic findings from 11 of these 80 individuals were previously published. In 76 (71.0%) individuals, the UHS phenotype were associated with pathogenic variants in PADI3. The 2 most commonly observed PADI3 variants account for 73 (48.0%) and 57 (37.5%) of the 152 variant PADI3 alleles in total, respectively. Two individuals carried pathogenic variants in TGM3, and 2 others carried pathogenic variants in TCHH. Haplotype analyses suggested a founder effect for the 4 most commonly observed pathogenic variants in the PADI3 gene.Conclusions and RelevanceThis cohort study extends and gives an overview of the genetic variant spectrum of UHS based on molecular genetic analyses of the largest worldwide collective of affected individuals, to our knowledge. Formerly, a diagnosis of UHS could only be made by physical examination of the patient and confirmed by microscopical examination of the hair shaft. The discovery of pathogenic variants in PADI3, TCHH, and TGM3 may open a new avenue for clinicians and affected individuals by introducing molecular diagnostics for UHS.

Published
2023

4. Assessment of the Genetic Spectrum of Uncombable Hair Syndrome in a Cohort of 107 Individuals

Author

Basmanav, F Buket, Cesarato, Nicole, Kumar, Sheetal, Borisov, Oleg, Kokordelis, Pavlos, Ralser, Damian J, Wehner, Maria, Axt, Daisy, Xiong, Xing, Thiele, Holger, Dolgin, Vadim, Gossmann, Yasmina, Fricker, Nadine, Dewenter, Malin Katharina, Weller, Karsten, Suri, Mohnish, Reichenbach, Herbert, Oji, Vinzenz, Addor, Marie-Claude, Ramirez, Karla, Stewart, Helen, Garcia Bartels, Natalie, Weibel, Lisa, Wagner, Nicola, George, Susannah, Kilic, Arzu, Tantcheva-Poór, Iliana, Stewart, Alison, Dikow, Nicola, Blaumeiser, Bettina, et al, and University of Zurich

Subjects
2708 Dermatology, 610 Medicine & health, 10220 Clinic for Surgery
Published
2022
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6. Assessment of the Genetic Spectrum of Uncombable Hair Syndrome in a Cohort of 107 Individuals

Author

Basmanav, F. Buket, primary, Cesarato, Nicole, additional, Kumar, Sheetal, additional, Borisov, Oleg, additional, Kokordelis, Pavlos, additional, Ralser, Damian J., additional, Wehner, Maria, additional, Axt, Daisy, additional, Xiong, Xing, additional, Thiele, Holger, additional, Dolgin, Vadim, additional, Gossmann, Yasmina, additional, Fricker, Nadine, additional, Dewenter, Malin Katharina, additional, Weller, Karsten, additional, Suri, Mohnish, additional, Reichenbach, Herbert, additional, Oji, Vinzenz, additional, Addor, Marie-Claude, additional, Ramirez, Karla, additional, Stewart, Helen, additional, Garcia Bartels, Natalie, additional, Weibel, Lisa, additional, Wagner, Nicola, additional, George, Susannah, additional, Kilic, Arzu, additional, Tantcheva-Poor, Iliana, additional, Stewart, Alison, additional, Dikow, Nicola, additional, Blaumeiser, Bettina, additional, Medvecz, Márta, additional, Blume-Peytavi, Ulrike, additional, Farrant, Paul, additional, Grimalt, Ramon, additional, Bertok, Sara, additional, Bradley, Lisa, additional, Eskin-Schwartz, Marina, additional, Birk, Ohad Samuel, additional, Bygum, Anette, additional, Simon, Michel, additional, Krawitz, Peter, additional, Fischer, Christine, additional, Hamm, Henning, additional, Fritz, Günter, additional, and Betz, Regina C., additional

Published
2022
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7. Further characterization of Borjeson‐Forssman‐Lehmann syndrome in females due to de novo variants in PHF6

Author

Gerber, Céline B., primary, Fliedner, Anna, additional, Bartsch, Oliver, additional, Berland, Siren, additional, Dewenter, Malin, additional, Haug, Marte, additional, Hayes, Ian, additional, Marin‐Reina, Purificacion, additional, Mark, Paul R., additional, Martinez‐Castellano, Francisco, additional, Maystadt, Isabelle, additional, Karadurmus, Deniz, additional, Steindl, Katharina, additional, Wiesener, Antje, additional, Zweier, Markus, additional, Sticht, Heinrich, additional, and Zweier, Christiane, additional

Published
2022
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8. Assessment of the Genetic Spectrum of Uncombable Hair Syndrome in a Cohort of 107 Individuals

Author

Basmanav, F. Buket, Cesarato, Nicole, Kumar, Sheetal, Borisov, Oleg, Kokordelis, Pavlos, Ralser, Damian J., Wehner, Maria, Axt, Daisy, Xiong, Xing, Thiele, Holger, Dolgin, Vadim, Gossmann, Yasmina, Fricker, Nadine, Dewenter, Malin Katharina, Weller, Karsten, Suri, Mohnish, Reichenbach, Herbert, Oji, Vinzenz, Addor, Marie-Claude, Ramirez, Karla, Stewart, Helen, Bartels, Natalie Garcia, Weibel, Lisa, Wagner, Nicola, George, Susannah, Kilic, Arzu, Tantcheva-Poor, Iliana, Stewart, Alison, Dikow, Nicola, Blaumeiser, Bettina, Medvecz, Marta, Blume-Peytavi, Ulrike, Farrant, Paul, Grimalt, Ramon, Bertok, Sara, Bradley, Lisa, Eskin-Schwartz, Marina, Birk, Ohad Samuel, Bygum, Anette, Simon, Michel, Krawitz, Peter, Fischer, Christine, Hamm, Henning, Fritz, Gunter, Betz, Regina C., Basmanav, F. Buket, Cesarato, Nicole, Kumar, Sheetal, Borisov, Oleg, Kokordelis, Pavlos, Ralser, Damian J., Wehner, Maria, Axt, Daisy, Xiong, Xing, Thiele, Holger, Dolgin, Vadim, Gossmann, Yasmina, Fricker, Nadine, Dewenter, Malin Katharina, Weller, Karsten, Suri, Mohnish, Reichenbach, Herbert, Oji, Vinzenz, Addor, Marie-Claude, Ramirez, Karla, Stewart, Helen, Bartels, Natalie Garcia, Weibel, Lisa, Wagner, Nicola, George, Susannah, Kilic, Arzu, Tantcheva-Poor, Iliana, Stewart, Alison, Dikow, Nicola, Blaumeiser, Bettina, Medvecz, Marta, Blume-Peytavi, Ulrike, Farrant, Paul, Grimalt, Ramon, Bertok, Sara, Bradley, Lisa, Eskin-Schwartz, Marina, Birk, Ohad Samuel, Bygum, Anette, Simon, Michel, Krawitz, Peter, Fischer, Christine, Hamm, Henning, Fritz, Gunter, and Betz, Regina C.

Abstract

Importance Uncombable hair syndrome (UHS) is a rare hair shaft anomaly that manifests during infancy and is characterized by dry, frizzy, and wiry hair that cannot be combed flat. Only about 100 known cases have been reported so far. Objective To elucidate the genetic spectrum of UHS. Design, Setting, and Participants This cohort study includes 107 unrelated index patients with a suspected diagnosis of UHS and family members who were recruited worldwide from January 2013 to December 2021. Participants of all ages, races, and ethnicities were recruited at referral centers or were enrolled on their own initiative following personal contact with the authors. Genetic analyses were conducted in Germany from January 2014 to December 2021. Main Outcomes and Measures Clinical photographs, Sanger or whole-exome sequencing and array-based genotyping of DNA extracted from blood or saliva samples, and 3-dimensional protein modeling. Descriptive statistics, such as frequency counts, were used to describe the distribution of identified pathogenic variants and genotypes. Results The genetic characteristics of patients with UHS were established in 80 of 107 (74.8%) index patients (82 [76.6%] female) who carried biallelic pathogenic variants in PADI3, TGM3, or TCHH (ie, genes that encode functionally related hair shaft proteins). Molecular genetic findings from 11 of these 80 individuals were previously published. In 76 (71.0%) individuals, the UHS phenotype were associated with pathogenic variants in PADI3. The 2 most commonly observed PADI3 variants account for 73 (48.0%) and 57 (37.5%) of the 152 variant PADI3 alleles in total, respectively. Two individuals carried pathogenic variants in TGM3, and 2 others carried pathogenic variants in TCHH. Haplotype analyses suggested a founder effect for the 4 most commonly observed pathogenic variants in the PADI3 gene. Conclusions and Relevance This cohort study extends and gives an overview of the genetic variant spectrum of UHS based on m

Published
2022

9. Structural mapping of GABRB3 variants reveals genotype-phenotype correlations

Author

Genetica Klinische Genetica, Genetica Oper. Mangt Genoom Diagnostiek, Brain, Child Health, Johannesen, Katrine M, Iqbal, Sumaiya, Guazzi, Milena, Mohammadi, Nazanin A, Pérez-Palma, Eduardo, Schaefer, Elise, De Saint Martin, Anne, Abiwarde, Marie Therese, McTague, Amy, Pons, Roser, Piton, Amelie, Kurian, Manju A, Ambegaonkar, Gautam, Firth, Helen, Sanchis-Juan, Alba, Deprez, Marie, Jansen, Katrien, De Waele, Liesbeth, Briltra, Eva H, Verbeek, Nienke E, van Kempen, Marjan, Fazeli, Walid, Striano, Pasquale, Zara, Federico, Visser, Gerhard, Braakman, Hilde M H, Haeusler, Martin, Elbracht, Miriam, Vaher, Ulvi, Smol, Thomas, Lemke, Johannes R, Platzer, Konrad, Kennedy, Joanna, Klein, Karl Martin, Au, Ping Yee Billie, Smyth, Kimberly, Kaplan, Julie, Thomas, Morgan, Dewenter, Malin K, Dinopoulos, Argirios, Campbell, Arthur J, Lal, Dennis, Lederer, Damien, Liao, Vivian W Y, Ahring, Philip K, Møller, Rikke S, Gardella, Elena, Genetica Klinische Genetica, Genetica Oper. Mangt Genoom Diagnostiek, Brain, Child Health, Johannesen, Katrine M, Iqbal, Sumaiya, Guazzi, Milena, Mohammadi, Nazanin A, Pérez-Palma, Eduardo, Schaefer, Elise, De Saint Martin, Anne, Abiwarde, Marie Therese, McTague, Amy, Pons, Roser, Piton, Amelie, Kurian, Manju A, Ambegaonkar, Gautam, Firth, Helen, Sanchis-Juan, Alba, Deprez, Marie, Jansen, Katrien, De Waele, Liesbeth, Briltra, Eva H, Verbeek, Nienke E, van Kempen, Marjan, Fazeli, Walid, Striano, Pasquale, Zara, Federico, Visser, Gerhard, Braakman, Hilde M H, Haeusler, Martin, Elbracht, Miriam, Vaher, Ulvi, Smol, Thomas, Lemke, Johannes R, Platzer, Konrad, Kennedy, Joanna, Klein, Karl Martin, Au, Ping Yee Billie, Smyth, Kimberly, Kaplan, Julie, Thomas, Morgan, Dewenter, Malin K, Dinopoulos, Argirios, Campbell, Arthur J, Lal, Dennis, Lederer, Damien, Liao, Vivian W Y, Ahring, Philip K, Møller, Rikke S, and Gardella, Elena

Published
2022

10. Further characterization of Borjeson-Forssman-Lehmann syndrome in females due to de novo variants in PHF6

Author

Gerber, Céline B, Fliedner, Anna, Bartsch, Oliver, Berland, Siren, Dewenter, Malin; https://orcid.org/0000-0001-8025-0736, Haug, Marte, Hayes, Ian, Marin‐Reina, Purificacion, Mark, Paul R, Martinez‐Castellano, Francisco, Maystadt, Isabelle, Karadurmus, Deniz, Steindl, Katharina; https://orcid.org/0000-0002-4425-3072, Wiesener, Antje, Zweier, Markus; https://orcid.org/0000-0001-8290-0413, Sticht, Heinrich; https://orcid.org/0000-0001-5644-045X, Zweier, Christiane, Gerber, Céline B, Fliedner, Anna, Bartsch, Oliver, Berland, Siren, Dewenter, Malin; https://orcid.org/0000-0001-8025-0736, Haug, Marte, Hayes, Ian, Marin‐Reina, Purificacion, Mark, Paul R, Martinez‐Castellano, Francisco, Maystadt, Isabelle, Karadurmus, Deniz, Steindl, Katharina; https://orcid.org/0000-0002-4425-3072, Wiesener, Antje, Zweier, Markus; https://orcid.org/0000-0001-8290-0413, Sticht, Heinrich; https://orcid.org/0000-0001-5644-045X, and Zweier, Christiane

Abstract

While inherited hemizygous variants in PHF6 cause X-linked recessive Borjeson-Forssman-Lehmann syndrome (BFLS) in males, de novo heterozygous variants in females are associated with an overlapping but distinct phenotype, including moderate to severe intellectual disability, characteristic facial dysmorphism, dental, finger and toe anomalies and linear skin pigmentation. By personal communication with colleagues, we assembled eleven additional females with BFLS due to variants in PHF6. We confirm the distinct phenotype to include variable intellectual disability, recognizable facial dysmorphism and other anomalies. We observed skewed X-inactivation in blood and streaky skin pigmentation compatible with functional mosaicism. Variants occurred de novo in ten individuals, of whom one was only mildly affected and transmitted it to her more severely affected daughter. The mutational spectrum comprises a 2-exon deletion, five truncating, one splice-site and three missense variants, the latter all located in the PHD2 domain and predicted to severely destabilize the domain structure. This observation supports the hypothesis of more severe variants in females contributing to gender-specific phenotypes in addition to or in combination with effects of X-inactivation and functional mosaicism. Therefore, our findings further delineate the clinical and mutational spectrum of female BFLS and provide further insights into possible genotype-phenotype correlations between females and males. Keywords: Borjeson-Forssman-Lehmann syndrome; PHF6; X-chromosomal; de novo.

Published
2022

11. Acral lamellar ichthyosis with amino acid substitution in the C-terminus of keratin 2.

Author

Frommherz, Leonie, Komlosi, Katalin, Hewel, Charlotte, Kopp, Julia, Dewenter, Malin, Zimmer, Andreas, Bartsch, Oliver, Linke, Matthias, Technau-Hafsi, Kristin, Gerber, Susanne, Fischer, Judith, and Has, Cristina

Subjects
ICHTHYOSIS, NUCLEOTIDE sequencing, AMINO acids, KERATIN, CHROMOSOME analysis, GENETIC variation
Abstract

Background: Most cases of hereditary ichthyoses present with generalized scaling and skin dryness. However, in some cases skin involvement is restricted to particular body regions as in acral lamellar ichthyosis. Objectives: We report on the genetic basis of acral ichthyosis in two families presenting with a similar phenotype. Methods: Genetic testing was performed by targeted next generation sequencing and whole-exome sequencing. For identity-by-descent analysis, the parents were genotyped and data analysis was performed with the Chromosome Analysis Suite Software. RT-PCR with RNA extracted from skin samples was used to analyse the effect of variants on splicing. Results: Genetic testing identified a few heterozygous variants, but only the variant in KRT2 c.1912T>C, p.Phe638Leu segregated with the disease and remained the strongest candidate. Pairwise identity-by-descent analysis revealed no indication of family relationship. Phenylalanine 638 is the second last amino acid upstream of the termination codon in the tail of K2, and substitution to leucine is predicted as probably damaging. Assessment of the variant is difficult, in part due to the lack of crystal structures of this region. Conclusions: Altogether, we show that a type of autosomal dominant acral ichthyosis is most probably caused by an amino acid substitution in the C-terminus of keratin 2. [ABSTRACT FROM AUTHOR]

Published
2023
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12. Structural mapping of GABRB3 variants reveals genotype-phenotype correlations

Author

Johannesen, Katrine M, primary, Iqbal, Sumaiya, additional, Guazzi, Milena, additional, Mohammadi, Nazanin A, additional, Pérez-Palma, Eduardo, additional, Schaefer, Elise, additional, De Saint Martin, Anne, additional, Abiwarde, Marie Therese, additional, McTague, Amy, additional, Pons, Roser, additional, Piton, Amelie, additional, Kurian, Manju A, additional, Ambegaonkar, Gautam, additional, Firth, Helen, additional, Sanchis-Juan, Alba, additional, Deprez, Marie, additional, Jansen, Katrien, additional, De Waele, Liesbeth, additional, Briltra, Eva H, additional, Verbeek, Nienke E, additional, van Kempen, Marjan, additional, Fazeli, Walid, additional, Striano, Pasquale, additional, Zara, Federico, additional, Visser, Gerhard, additional, Braakman, Hilde M H, additional, Haeusler, Martin, additional, Elbracht, Miriam, additional, Sternman, David, additional, Vaher, Ulvi, additional, Smol, Thomas, additional, Lemke, Johannes R, additional, Platzer, Konrad, additional, Kennedy, Joanna, additional, Klein, Karl Martin, additional, Billie Au, Ping Yee, additional, Smyth, Kimberly, additional, Kaplan, Julie, additional, Thomas, Morgan, additional, Dewenter, Malin K, additional, Dinopoulos, Argirios, additional, Campbell, Arthur J, additional, Lal, Dennis, additional, Lederer, Damien, additional, Liao, Vivian W Y, additional, Ahring, Philip K, additional, Møller, Rikke S., additional, and Gardella, Elena, additional

Published
2021
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13. Structural mapping of GABRB3variants reveals genotype–phenotype correlations

Author

Johannesen, Katrine M., Iqbal, Sumaiya, Guazzi, Milena, Mohammadi, Nazanin A., Pérez-Palma, Eduardo, Schaefer, Elise, De Saint Martin, Anne, Abiwarde, Marie Therese, McTague, Amy, Pons, Roser, Piton, Amelie, Kurian, Manju A., Ambegaonkar, Gautam, Firth, Helen, Sanchis-Juan, Alba, Deprez, Marie, Jansen, Katrien, De Waele, Liesbeth, Briltra, Eva H., Verbeek, Nienke E., van Kempen, Marjan, Fazeli, Walid, Striano, Pasquale, Zara, Federico, Visser, Gerhard, Braakman, Hilde M.H., Haeusler, Martin, Elbracht, Miriam, Vaher, Ulvi, Smol, Thomas, Lemke, Johannes R., Platzer, Konrad, Kennedy, Joanna, Klein, Karl Martin, Au, Ping Yee Billie, Smyth, Kimberly, Kaplan, Julie, Thomas, Morgan, Dewenter, Malin K., Dinopoulos, Argirios, Campbell, Arthur J., Lal, Dennis, Lederer, Damien, Liao, Vivian W.Y., Ahring, Philip K., Møller, Rikke S., and Gardella, Elena

Abstract

Pathogenic variants in GABRB3have been associated with a spectrum of phenotypes from severe developmental disorders and epileptic encephalopathies to milder epilepsy syndromes and mild intellectual disability (ID). In this study, we analyzed a large cohort of individuals with GABRB3variants to deepen the phenotypic understanding and investigate genotype–phenotype correlations.

Published
2022
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