| Literature DB >> 30905398 |
Felix Marbach1, Cecilie F Rustad2, Angelika Riess3, Dejan Đukić4, Tzung-Chien Hsieh5, Itamar Jobani6, Trine Prescott7, Andrea Bevot8, Florian Erger1, Gunnar Houge9, Maria Redfors10, Janine Altmueller11, Tomasz Stokowy12, Christian Gilissen13, Christian Kubisch14, Emanuela Scarano15, Laura Mazzanti15, Torunn Fiskerstrand9, Peter M Krawitz5, Davor Lessel14, Christian Netzer16.
Abstract
Over a relatively short period of time, the clinical geneticist's "toolbox" has been expanded by machine-learning algorithms for image analysis, which can be applied to the task of syndrome identification on the basis of facial photographs, but these technologies harbor potential beyond the recognition of established phenotypes. Here, we comprehensively characterized two individuals with a hitherto unknown genetic disorder caused by the same de novo mutation in LEMD2 (c.1436C>T;p.Ser479Phe), the gene which encodes the nuclear envelope protein LEM domain-containing protein 2 (LEMD2). Despite different ages and ethnic backgrounds, both individuals share a progeria-like facial phenotype and a distinct combination of physical and neurologic anomalies, such as growth retardation; hypoplastic jaws crowded with multiple supernumerary, yet unerupted, teeth; and cerebellar intention tremor. Immunofluorescence analyses of patient fibroblasts revealed mutation-induced disturbance of nuclear architecture, recapitulating previously published data in LEMD2-deficient cell lines, and additional experiments suggested mislocalization of mutant LEMD2 protein within the nuclear lamina. Computational analysis of facial features with two different deep neural networks showed phenotypic proximity to other nuclear envelopathies. One of the algorithms, when trained to recognize syndromic similarity (rather than specific syndromes) in an unsupervised approach, clustered both individuals closely together, providing hypothesis-free hints for a common genetic etiology. We show that a recurrent de novo mutation in LEMD2 causes a nuclear envelopathy whose prognosis in adolescence is relatively good in comparison to that of classical Hutchinson-Gilford progeria syndrome, and we suggest that the application of artificial intelligence to the analysis of patient images can facilitate the discovery of new genetic disorders.Entities:
Keywords: LEM domain-containing protein 2”; “deep neuronal network” and “intra-syndromal similarity; “next-generation phenotyping”; “nuclear envelopathy”; “progeria-like”
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Year: 2019 PMID: 30905398 PMCID: PMC6451726 DOI: 10.1016/j.ajhg.2019.02.021
Source DB: PubMed Journal: Am J Hum Genet ISSN: 0002-9297 Impact factor: 11.025