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Wilson disease (novel ATP7B variants) with concomitant FLNC-related cardiomyopathy. 威尔逊病（新型 ATP7B 变异）并发 FLNC 相关心肌病。
IF 1
Human Genome Variation Pub Date : 2024-08-29 DOI: 10.1038/s41439-024-00283-y
Takeshi Imai, Satomi Mitsuhashi, Kenji Isahaya, Soichiro Shibata, Yosuke Kawai, Yosuke Omae, Katsushi Tokunaga, Yoshihisa Yamano
{"title":"Wilson disease (novel ATP7B variants) with concomitant FLNC-related cardiomyopathy.","authors":"Takeshi Imai, Satomi Mitsuhashi, Kenji Isahaya, Soichiro Shibata, Yosuke Kawai, Yosuke Omae, Katsushi Tokunaga, Yoshihisa Yamano","doi":"10.1038/s41439-024-00283-y","DOIUrl":"10.1038/s41439-024-00283-y","url":null,"abstract":"<p><p>We report a case of Wilson disease (WD) with dilated cardiomyopathy in which whole-genome sequencing (WGS) revealed the rare co-occurrence of two novel compound heterozygous ATP7B pathogenic variants (NM_001005918.3:c.2250del/p.N751Tfs*9 and c.3496C>T/p.L1166F) and a known FLNC pathogenic variant. Our results highlight the usefulness of WGS, even in the diagnosis of well-characterized genetic diseases such as WD.</p>","PeriodicalId":36861,"journal":{"name":"Human Genome Variation","volume":"11 1","pages":"34"},"PeriodicalIF":1.0,"publicationDate":"2024-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11362149/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142113019","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Missense BICD2 variants in fetuses with congenital arthrogryposis and pterygia. 患有先天性关节突眼和翼状胬肉的胎儿中的错义 BICD2 变异。
IF 1
Human Genome Variation Pub Date : 2024-08-26 DOI: 10.1038/s41439-024-00290-z
Layla Masuda, Akihiro Hasegawa, Hiromi Kamura, Fuyuki Hasegawa, Michihiro Yamamura, Kosuke Taniguchi, Yuki Ito, Kenichiro Hata, Osamu Samura, Aikou Okamoto
{"title":"Missense BICD2 variants in fetuses with congenital arthrogryposis and pterygia.","authors":"Layla Masuda, Akihiro Hasegawa, Hiromi Kamura, Fuyuki Hasegawa, Michihiro Yamamura, Kosuke Taniguchi, Yuki Ito, Kenichiro Hata, Osamu Samura, Aikou Okamoto","doi":"10.1038/s41439-024-00290-z","DOIUrl":"10.1038/s41439-024-00290-z","url":null,"abstract":"<p><p>Type 2 spinal muscular atrophy with lower extremity dominance (SMALED2) is caused by bicaudal D cargo adaptor 2 (BICD2) variants. However, the SMALED2 genotype and phenotype correlation have not been thoroughly characterized. We identified de novo heterozygous BICD2 missense variants in two fetuses with severe, prenatally diagnosed multiple arthrogryposis congenita. This report provides further insights into the genetics of this rare disease.</p>","PeriodicalId":36861,"journal":{"name":"Human Genome Variation","volume":"11 1","pages":"32"},"PeriodicalIF":1.0,"publicationDate":"2024-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11345410/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142056752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
A case of severe Aicardi-Goutières syndrome with a homozygous RNASEH2B intronic variant. 一例患有同型 RNASEH2B 内含子变异的重度艾卡迪-古蒂耶尔综合征病例。
IF 1
Human Genome Variation Pub Date : 2024-08-26 DOI: 10.1038/s41439-024-00291-y
Yuri Shibata, Akimichi Shibata, Takeshi Mizuguchi, Naomichi Matsumoto, Hitoshi Osaka
{"title":"A case of severe Aicardi-Goutières syndrome with a homozygous RNASEH2B intronic variant.","authors":"Yuri Shibata, Akimichi Shibata, Takeshi Mizuguchi, Naomichi Matsumoto, Hitoshi Osaka","doi":"10.1038/s41439-024-00291-y","DOIUrl":"10.1038/s41439-024-00291-y","url":null,"abstract":"<p><p>We report a case of severe Aicardi-Goutières syndrome caused by a novel homozygous RNASEH2B intronic variant, NC_000013.10(NM_024570.4):c.65-13G > A p.Glu22Valfs*5. The patient was born with pseudo-TORCH symptoms, including intracranial calcification, cataracts, and hepatosplenomegaly. Furthermore, the patient exhibited profound intellectual impairment and died at 14 months due to aspiration pneumonia accompanied by interstitial lung abnormalities. The severity of the patient's symptoms underscores the critical role of the C-terminal region of RNase H2B.</p>","PeriodicalId":36861,"journal":{"name":"Human Genome Variation","volume":"11 1","pages":"33"},"PeriodicalIF":1.0,"publicationDate":"2024-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11345432/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142056751","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Uniparental maternal tetrasomy X co-occurrence with paternal nondisjunction: investigation of the origin of 48,XXXX. 单亲母系 X 四体综合征与父系非连接共同发生：48,XXXX 的起源调查。
IF 1
Human Genome Variation Pub Date : 2024-08-16 DOI: 10.1038/s41439-024-00289-6
Keiko Shimojima Yamamoto, Sakurako Yamamoto, Taichi Imaizumi, Satoko Kumada, Toshiyuki Yamamoto
{"title":"Uniparental maternal tetrasomy X co-occurrence with paternal nondisjunction: investigation of the origin of 48,XXXX.","authors":"Keiko Shimojima Yamamoto, Sakurako Yamamoto, Taichi Imaizumi, Satoko Kumada, Toshiyuki Yamamoto","doi":"10.1038/s41439-024-00289-6","DOIUrl":"10.1038/s41439-024-00289-6","url":null,"abstract":"<p><p>Tetrasomy X or 48,XXXX is a rare sex chromosome aneuploidy. The parental origin of tetrasomy X in a female patient with developmental delay was analyzed; all four X chromosomes were derived from the mother, and there were no paternally derived sex chromosomes. This finding indicates a rare incidental co-occurrence of maternal and paternal nondisjunction or polysomy rescue. The mechanism of 48,XXYY, which is related to developmental delay in males, was analyzed for comparison.</p>","PeriodicalId":36861,"journal":{"name":"Human Genome Variation","volume":"11 1","pages":"31"},"PeriodicalIF":1.0,"publicationDate":"2024-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11329761/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141996617","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The APOA1 p.Leu202Arg variant potentially causes autosomal recessive cardiac amyloidosis. APOA1 p.Leu202Arg 变异可能导致常染色体隐性遗传性心脏淀粉样变性病。
IF 1
Human Genome Variation Pub Date : 2024-08-16 DOI: 10.1038/s41439-024-00288-7
Shusuke Yagi, Ryosuke Miyamoto, Masayoshi Tasaki, Hiroyuki Morino, Ryuji Otani, Muneyuki Kadota, Takayuki Ise, Hiroki Yamazaki, Kenya Kusunose, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Daiju Fukuda, Mitsuharu Ueda, Masataka Sata
{"title":"The APOA1 p.Leu202Arg variant potentially causes autosomal recessive cardiac amyloidosis.","authors":"Shusuke Yagi, Ryosuke Miyamoto, Masayoshi Tasaki, Hiroyuki Morino, Ryuji Otani, Muneyuki Kadota, Takayuki Ise, Hiroki Yamazaki, Kenya Kusunose, Koji Yamaguchi, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Daiju Fukuda, Mitsuharu Ueda, Masataka Sata","doi":"10.1038/s41439-024-00288-7","DOIUrl":"10.1038/s41439-024-00288-7","url":null,"abstract":"<p><p>ApoA-I amyloidosis is an extremely rare form of systemic amyloidosis that commonly involves the heart, kidneys, and liver. ApoA-I amyloidosis is caused by amyloidogenic variants of APOA1 that are inherited in an autosomal dominant manner. Here, we report a 69-year-old man with sporadic cardiac amyloidosis who was born to consanguineous parents and carried a homozygous variant of p.Leu202Arg in APOA1.</p>","PeriodicalId":36861,"journal":{"name":"Human Genome Variation","volume":"11 1","pages":"30"},"PeriodicalIF":1.0,"publicationDate":"2024-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11329782/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141996616","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Intermediate phenotype between CMT2Z and DIGFAN associated with a novel MORC2 variant: a case report. 与新型 MORC2 变异相关的 CMT2Z 和 DIGFAN 之间的中间表型：一份病例报告。
IF 1
Human Genome Variation Pub Date : 2024-08-15 DOI: 10.1038/s41439-024-00287-8
Kenta Hanada, Yusuke Osaki, Ryosuke Miyamoto, Kohei Muto, Shotaro Haji, Keyoumu Nazere, Yuki Kuwano, Hiroyuki Morino, Yoshiteru Azuma, Satoko Miyatake, Naomichi Matsumoto, Yuishin Izumi
{"title":"Intermediate phenotype between CMT2Z and DIGFAN associated with a novel MORC2 variant: a case report.","authors":"Kenta Hanada, Yusuke Osaki, Ryosuke Miyamoto, Kohei Muto, Shotaro Haji, Keyoumu Nazere, Yuki Kuwano, Hiroyuki Morino, Yoshiteru Azuma, Satoko Miyatake, Naomichi Matsumoto, Yuishin Izumi","doi":"10.1038/s41439-024-00287-8","DOIUrl":"10.1038/s41439-024-00287-8","url":null,"abstract":"<p><p>Charcot-Marie-Tooth disease type 2Z is caused by MORC2 mutations and presents with axonal neuropathy. MORC2 mutations can also manifest as developmental delay, impaired growth, dysmorphic facies, and axonal neuropathy (DIGFAN). We report a patient exhibiting an intermediate phenotype between these diseases associated with a novel MORC2 variant. A literature review revealed that the genotype‒phenotype correlation in MORC2-related disorders is complex and that the same mutation can cause a variety of phenotypes.</p>","PeriodicalId":36861,"journal":{"name":"Human Genome Variation","volume":"11 1","pages":"29"},"PeriodicalIF":1.0,"publicationDate":"2024-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11324651/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141983449","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Investigation of a novel PROS1 splicing variant in a patient with protein S deficiency. 研究一名蛋白 S 缺乏症患者的新型 PROS1 剪接变体。
IF 1
Human Genome Variation Pub Date : 2024-07-26 DOI: 10.1038/s41439-024-00286-9
Yo Niida, Wataru Fujita, Sumihito Togi, Hiroki Ura
{"title":"Investigation of a novel PROS1 splicing variant in a patient with protein S deficiency.","authors":"Yo Niida, Wataru Fujita, Sumihito Togi, Hiroki Ura","doi":"10.1038/s41439-024-00286-9","DOIUrl":"10.1038/s41439-024-00286-9","url":null,"abstract":"<p><p>Here, we report a novel PROS1 splicing mutation in a patient with type I protein S deficiency. Qualitative and quantitative analysis of pathogenic splicing variants at the mRNA level was performed by long-range PCR-based targeted DNA and RNA sequencing. A base substitution in the exon 4 splicing donor site activates a potential splicing donor site in intron 4, resulting in an in-frame insertion of 48 bases (16 amino acids).</p>","PeriodicalId":36861,"journal":{"name":"Human Genome Variation","volume":"11 1","pages":"28"},"PeriodicalIF":1.0,"publicationDate":"2024-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11282053/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141767526","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Homozygous 6-bp deletion of IGFALS in a prepubertal boy with short stature. 一名青春期前身材矮小男孩的 IGFALS 基因出现 6-bp 缺失。
IF 1
Human Genome Variation Pub Date : 2024-07-26 DOI: 10.1038/s41439-024-00285-w
Hibiki Doi, Ikuko Kageyama, Yuko Katoh-Fukui, Atsushi Hattori, Maki Fukami, Naoto Shimura
{"title":"Homozygous 6-bp deletion of IGFALS in a prepubertal boy with short stature.","authors":"Hibiki Doi, Ikuko Kageyama, Yuko Katoh-Fukui, Atsushi Hattori, Maki Fukami, Naoto Shimura","doi":"10.1038/s41439-024-00285-w","DOIUrl":"10.1038/s41439-024-00285-w","url":null,"abstract":"<p><p>Biallelic IGFALS variants lead to acid‒labile subunit (ALS) deficiency characterized by growth hormone resistance with or without delayed puberty. Here, we report a prepubertal boy with a homozygous 2-amino acid deletion within the fourth N-glycosylation motif (c.1103_1108del, p.N368_S370delinsT) associated with parental consanguinity. He showed short stature consistent with ALS deficiency. This case expands the mutation spectrum of IGFALS to include the elimination of only one N-glycosylation motif of ALS.</p>","PeriodicalId":36861,"journal":{"name":"Human Genome Variation","volume":"11 1","pages":"27"},"PeriodicalIF":1.0,"publicationDate":"2024-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11282113/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141767525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
TACSTD2 in gelatinous drop-like corneal dystrophy: variant functional analysis and expression in the cornea after limbal stem cell transplantation. 胶样角膜营养不良症中的TACSTD2：变体功能分析和角膜缘干细胞移植后的表达。
IF 1
Human Genome Variation Pub Date : 2024-07-16 DOI: 10.1038/s41439-024-00284-x
Liubov O Skorodumova, Ekaterina N Grafskaia, Daria D Kharlampieva, Dmitry I Maltsev, Tatiana V Petrova, Alexandra V Kanygina, Elena V Fedoseeva, Pavel V Makarov, Boris E Malyugin
{"title":"TACSTD2 in gelatinous drop-like corneal dystrophy: variant functional analysis and expression in the cornea after limbal stem cell transplantation.","authors":"Liubov O Skorodumova, Ekaterina N Grafskaia, Daria D Kharlampieva, Dmitry I Maltsev, Tatiana V Petrova, Alexandra V Kanygina, Elena V Fedoseeva, Pavel V Makarov, Boris E Malyugin","doi":"10.1038/s41439-024-00284-x","DOIUrl":"10.1038/s41439-024-00284-x","url":null,"abstract":"<p><p>Gelatinous drop-like corneal dystrophy (GDLD) is a rare autosomal recessive eye disease. GDLD is characterized by the loss of barrier function in corneal epithelial cells (CECs) and amyloid deposition due to pathogenic variants in the TACSTD2 gene. Limbal stem cell transplantation (LSCT) has been suggested as an effective therapeutic alternative for patients with GDLD. However, despite LSCT, amyloid deposition recurs in some patients. The pathogenesis of recurrence is poorly studied. We present the case of a patient with GDLD. Genetic analysis revealed a homozygous deletion, NM_002353.3:c.653del, in the TACSTD2 gene. Functional analysis in a cell model system revealed the loss of the transmembrane domain and subcellular protein mislocalization. The patient with GDLD underwent direct allogeneic LSCT with epithelial debridement followed by deep anterior lamellar keratoplasty 10 months later due to amyloid deposition and deterioration of vision. Taken together, the results of transcriptome analysis and immunofluorescence staining of post-LSCT corneal sample with amyloid deposits obtained during keratoplasty demonstrated complete restoration of wild-type TACSTD2 expression, indicating that donor CECs replaced host CECs. Our study provides experimental evidence that amyloid deposition can recur after LSCT despite complete restoration of wild-type TACSTD2 expression.</p>","PeriodicalId":36861,"journal":{"name":"Human Genome Variation","volume":"11 1","pages":"26"},"PeriodicalIF":1.0,"publicationDate":"2024-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11252363/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141627951","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Identifying unstable CNG repeat loci in the human genome: a heuristic approach and implications for neurological disorders. 识别人类基因组中不稳定的 CNG 重复位点：启发式方法及其对神经系统疾病的影响。
IF 1
Human Genome Variation Pub Date : 2024-06-13 DOI: 10.1038/s41439-024-00281-0
Varun Suroliya, Bharathram Uppili, Manish Kumar, Vineet Jha, Achal K Srivastava, Mohammed Faruq
{"title":"Identifying unstable CNG repeat loci in the human genome: a heuristic approach and implications for neurological disorders.","authors":"Varun Suroliya, Bharathram Uppili, Manish Kumar, Vineet Jha, Achal K Srivastava, Mohammed Faruq","doi":"10.1038/s41439-024-00281-0","DOIUrl":"10.1038/s41439-024-00281-0","url":null,"abstract":"<p><p>Tandem nucleotide repeat (TNR) expansions, particularly the CNG nucleotide configuration, are associated with a variety of neurodegenerative disorders. In this study, we aimed to identify novel unstable CNG repeat loci associated with the neurogenetic disorder spinocerebellar ataxia (SCA). Using a computational approach, 15,069 CNG repeat loci in the coding and noncoding regions of the human genome were identified. Based on the feature selection criteria (repeat length >10 and functional location of repeats), we selected 52 repeats for further analysis and evaluated the repeat length variability in 100 control subjects. A subset of 19 CNG loci observed to be highly variable in control subjects was selected for subsequent analysis in 100 individuals with SCA. The genes with these highly variable repeats also exhibited higher gene expression levels in the brain according to the tissue expression dataset (GTEx). No pathogenic expansion events were identified in patient samples, which is a limitation given the size of the patient group examined; however, these loci contain potential risk alleles for expandability. Recent studies have implicated GLS, RAI1, GIPC1, MED15, EP400, MEF2A, and CNKSR2 in neurological diseases, with GLS, GIPC1, MED15, RAI1, and MEF2A sharing the same repeat loci reported in this study. This finding validates the approach of evaluating repeat loci in different populations and their possible implications for human pathologies.</p>","PeriodicalId":36861,"journal":{"name":"Human Genome Variation","volume":"11 1","pages":"25"},"PeriodicalIF":1.0,"publicationDate":"2024-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11176344/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141318478","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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