Blood · 2019
EFL1 mutations impair eIF6 release to cause Shwachman-Diamond syndrome.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Tan Shengjiang, Kermasson Laëtitia, Hoslin Angela, Jaako Pekka, Faille Alexandre, Acevedo-Arozena Abraham, Lengline Etienne, Ranta Dana, Poirée Maryline, Fenneteau Odile, Ducou le Pointe Hubert, Fumagalli Stefano, Beaupain Blandine, Nitschké Patrick, Bôle-Feysot Christine, de Villartay Jean-Pierre, Bellanné-Chantelot Christine, Donadieu Jean, Kannengiesser Caroline, Warren Alan J, Revy Patrick
Аннотация
Shwachman-Diamond syndrome (SDS) is a recessive disorder typified by bone marrow failure and predisposition to hematological malignancies. SDS is predominantly caused by deficiency of the allosteric regulator Shwachman-Bodian-Diamond syndrome that cooperates with elongation factor-like GTPase 1 (EFL1) to catalyze release of the ribosome antiassociation factor eIF6 and activate translation. Here, we report biallelic mutations in EFL1 in 3 unrelated individuals with clinical features of SDS. Cellular defects in these individuals include impaired ribosomal subunit joining and attenuated global protein translation as a consequence of defective eIF6 eviction. In mice, Efl1 deficiency recapitulates key aspects of the SDS phenotype. By identifying biallelic EFL1 mutations in SDS, we define this leukemia predisposition disorder as a ribosomopathy that is caused by corruption of a fundamental, conserved mechanism, which licenses entry of the large ribosomal subunit into translation.
Предметные рубрики MeSH
AdolescentAnimalsCells, CulturedDNA Mutational AnalysisDisease Models, AnimalDisease SusceptibilityFemaleGenome-Wide Association StudyHumansInfantMaleMiceMice, TransgenicModels, MolecularMutationPedigreePeptide Elongation FactorsPeptide Initiation FactorsPhenotypeProtein ConformationRibonucleoprotein, U5 Small NuclearShwachman-Diamond SyndromeStructure-Activity RelationshipWhole Genome Sequencing