Literature DB >> 33517444

Genotype & phenotype in Lowe Syndrome: specific OCRL1 patient mutations differentially impact cellular phenotypes.

Swetha Ramadesikan1, Lisette Skiba1, Jennifer Lee1, Kayalvizhi Madhivanan1, Daipayan Sarkar1, Agustina De La Fuente1, Claudia B Hanna1, Genki Terashi1, Tony Hazbun2, Daisuke Kihara1,3, R Claudio Aguilar1.   

Abstract

Lowe Syndrome (LS) is a lethal genetic disorder caused by mutations in the OCRL1 gene which encodes the lipid 5' phosphatase Ocrl1. Patients exhibit a characteristic triad of symptoms including eye, brain and kidney abnormalities with renal failure as the most common cause of premature death. Over 200 OCRL1 mutations have been identified in LS, but their specific impact on cellular processes is unknown. Despite observations of heterogeneity in patient symptom severity, there is little understanding of the correlation between genotype and its impact on phenotype. Here, we show that different mutations had diverse effects on protein localization and on triggering LS cellular phenotypes. In addition, some mutations affecting specific domains imparted unique characteristics to the resulting mutated protein. We also propose that certain mutations conformationally affect the 5'-phosphatase domain of the protein, resulting in loss of enzymatic activity and causing common and specific phenotypes (a conformational disease scenario). This study is the first to show the differential effect of patient 5'-phosphatase mutations on cellular phenotypes and introduces a conformational disease component in LS. This work provides a framework that explains symptom heterogeneity and can help stratify patients as well as to produce a more accurate prognosis depending on the nature and location of the mutation within the OCRL1 gene.
© The Author(s) 2021. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.

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Year:  2021        PMID: 33517444      PMCID: PMC8091038          DOI: 10.1093/hmg/ddab025

Source DB:  PubMed          Journal:  Hum Mol Genet        ISSN: 0964-6906            Impact factor:   6.150


  71 in total

1.  The Lowe's oculocerebrorenal syndrome gene encodes a protein highly homologous to inositol polyphosphate-5-phosphatase.

Authors:  O Attree; I M Olivos; I Okabe; L C Bailey; D L Nelson; R A Lewis; R R McInnes; R L Nussbaum
Journal:  Nature       Date:  1992-07-16       Impact factor: 49.962

2.  Ocrl1, a PtdIns(4,5)P(2) 5-phosphatase, is localized to the trans-Golgi network of fibroblasts and epithelial cells.

Authors:  M A Dressman; I M Olivos-Glander; R L Nussbaum; S F Suchy
Journal:  J Histochem Cytochem       Date:  2000-02       Impact factor: 2.479

Review 3.  Inositol 5-phosphatases: insights from the Lowe syndrome protein OCRL.

Authors:  Michelle Pirruccello; Pietro De Camilli
Journal:  Trends Biochem Sci       Date:  2012-02-28       Impact factor: 13.807

4.  A structural basis for Lowe syndrome caused by mutations in the Rab-binding domain of OCRL1.

Authors:  Xiaomin Hou; Nina Hagemann; Stefan Schoebel; Wulf Blankenfeldt; Roger S Goody; Kai S Erdmann; Aymelt Itzen
Journal:  EMBO J       Date:  2011-03-04       Impact factor: 11.598

5.  CHARMM-GUI Membrane Builder for Complex Biological Membrane Simulations with Glycolipids and Lipoglycans.

Authors:  Jumin Lee; Dhilon S Patel; Jonas Ståhle; Sang-Jun Park; Nathan R Kern; Seonghoon Kim; Joonseong Lee; Xi Cheng; Miguel A Valvano; Otto Holst; Yuriy A Knirel; Yifei Qi; Sunhwan Jo; Jeffery B Klauda; Göran Widmalm; Wonpil Im
Journal:  J Chem Theory Comput       Date:  2018-12-28       Impact factor: 6.006

6.  Lowe syndrome protein OCRL1 interacts with clathrin and regulates protein trafficking between endosomes and the trans-Golgi network.

Authors:  Rawshan Choudhury; Aipo Diao; Fang Zhang; Evan Eisenberg; Agnes Saint-Pol; Catrin Williams; Athanasios Konstantakopoulos; John Lucocq; Ludger Johannes; Catherine Rabouille; Lois E Greene; Martin Lowe
Journal:  Mol Biol Cell       Date:  2005-05-25       Impact factor: 4.138

7.  Golgin-84-associated Golgi fragmentation triggers tau hyperphosphorylation by activation of cyclin-dependent kinase-5 and extracellular signal-regulated kinase.

Authors:  Qian Jiang; Lu Wang; Yang Guan; Hui Xu; Yi Niu; Li Han; Yu-Ping Wei; Li Lin; Jiang Chu; Qun Wang; Ying Yang; Lei Pei; Jian-Zhi Wang; Qing Tian
Journal:  Neurobiol Aging       Date:  2013-11-28       Impact factor: 4.673

8.  Lowe syndrome patient cells display mTOR- and RhoGTPase-dependent phenotypes alleviated by rapamycin and statins.

Authors:  Kayalvizhi Madhivanan; Swetha Ramadesikan; Wen-Chieh Hsieh; Mariana C Aguilar; Claudia B Hanna; Robert L Bacallao; R Claudio Aguilar
Journal:  Hum Mol Genet       Date:  2020-06-27       Impact factor: 6.150

9.  Lowe syndrome, a deficiency of phosphatidylinositol 4,5-bisphosphate 5-phosphatase in the Golgi apparatus.

Authors:  S F Suchy; I M Olivos-Glander; R L Nussabaum
Journal:  Hum Mol Genet       Date:  1995-12       Impact factor: 6.150

10.  Species-specific difference in expression and splice-site choice in Inpp5b, an inositol polyphosphate 5-phosphatase paralogous to the enzyme deficient in Lowe Syndrome.

Authors:  Susan P Bothwell; Leslie W Farber; Adam Hoagland; Robert L Nussbaum
Journal:  Mamm Genome       Date:  2010-09-26       Impact factor: 2.957

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  1 in total

1.  The Future of Genetic Disease Studies: Assembling an Updated Multidisciplinary Toolbox.

Authors:  Swetha Ramadesikan; Jennifer Lee; Ruben Claudio Aguilar
Journal:  Front Cell Dev Biol       Date:  2022-04-28
  1 in total

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