Restoration of F508-del Function by Transcomplementation: The Partners Meet in the Endoplasmic Reticulum

Emily Anne Smith Bergbower; Inna B. Sabirzhanova; Clément Boinot; William B. Guggino; Liudmila Cebotaru

doi:10.33594/000000089

Cited by 5Cystic Fibrosis Research AdvancesVirus-based gene therapy researchRNA Interference and Gene Delivery

Restoration of F508-del Function by Transcomplementation: The Partners Meet in the Endoplasmic Reticulum

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Emily Anne Smith Bergbower, Inna B. Sabirzhanova, Clément Boinot, William B. Guggino, Liudmila Cebotaru·2019·Cellular Physiology and Biochemistry

DOI 10.33594/000000089PMC PMC7097968

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Abstract

Background/Aims: Because of the small size of adeno-associated virus, AAV, the cystic fibrosis conductance regulator, CFTR, cDNA is too large to fit within AAV and must be truncated.We report here on two truncated versions of CFTR, which, when inserted into AAV1 and used to infect airway cells, rescue F508-del CFTR via transcomplementation.The purpose of this study is to shed light on where in the cell transcomplementation occurs and how it results in close association between the endogenous F508-del and truncated CFTR.Methods: We treated CF airway cells (CFBE41o -) with AAV2/1 (AAV2 inverted terminal repeats/AAV1 capsid) containing truncated forms of CFTR, ∆264 and ∆27-264 CFTR, who can restore the function of F508-del by transcomplementation.We addressed the aims of the study using a combination of confocal microscopy and short circuit currents measurements.For the latter, CF bronchial epithelial cells (CFBE) were grown on permeable supports.Results: We show that both F508del and the truncation mutants colocalize in the ER and that both the rescued F508-del and the transcomplementing mutants reach the plasma membrane together.There was significant fluorescence resonance energy transfer (FRET) between F508-del and the transcomplementing mutants within the endoplasmic reticulum (ER), suggesting that transcomplementation occurs through a bimolecular interaction.We found that transcomplementation could increase the Isc in CFBE41o -cells stably expressing additional wt-CFTR or F508-del and in parental CFBE41o -cells expressing endogenous levels of F508-del.Conclusion: We conclude that the functional rescue of F508-del by transcomplementation occurs via a bimolecular interaction that most likely begins in the ER and continues at the plasma membrane.These results come at an opportune time for developing a gene therapy for CF and offer new treatment options for a wide range of CF patients.

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For cystic fibrosis, the functionality of the CFTR protein affected by the F508del mutation could be restored following AAV-mediated administration of truncated CFTR variants as a result of a biomolecular interaction that stabilized the endogenous protein otherwise destined to rapid degradation.
“This was shown, for instance, for cystic fibrosis, where the functionality of the Cystic Fibrosis Transmembrane conductance Regulator (CFTR) protein affected by the F508del mutation could be restored following AAV-mediated administration of truncated CFTR variants as a result of a biomolecular interaction that stabilized the endogenous protein otherwise destined to rapid degradation [73].”
From Circumventing the packaging limit of AAV-mediated gene replacement therapy for neurological disorders (2022) · cites this paper as [73]
In certain contexts, delivery of truncated proteins can rescue the defective/dysfunctional endogenous protein by a phenomenon called 'transcomplementation'.
“Interestingly, it has been shown that in certain contexts, the delivery of truncated proteins can rescue the defective/dysfunctional endogenous protein by a phenomenon called 'transcomplementation.'”
From Circumventing the packaging limit of AAV-mediated gene replacement therapy for neurological disorders (2022) · cites this paper as [73]

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Circumventing the packaging limit of AAV-mediated gene replacement therapy for neurological disorders
Marrone, L., Marchi, P. M., & Azzouz, M. (2022) · Expert Opinion on Biological Therapy · doi:10.1080/14712598.2022.2012148 · Cited by 56 · see citing works
“restored following AAV-mediated administration of truncated CFTR variants as a result of a biomolecular interaction that stabilized the endogenous protein otherwise destined to rapid degradation [73].”
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Complement yourself: transcomplementation rescues partially folded mutant proteins
Cebotaru, L., & Guggino, W. B. (2014) · Biophysical Reviews · doi:10.1007/s12551-014-0137-3 · Cited by 10 · see citing works
Self-citation
Transcomplementation by a Truncation Mutant of Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) Enhances ΔF508 Processing through a Biomolecular Interaction
Cebotaru, L., Woodward, O. M., Cebotaru, V., & Guggino, W. B. (2013) · Journal of Biological Chemistry · doi:10.1074/jbc.m112.420489 · Cited by 20 · see citing works
Self-citation
A truncated CFTR protein rescues endogenous ∆F508‐CFTR and corrects chloride transport in mice
Cormet‐Boyaka, E., Hong, J. S., Berdiev, B. K., Fortenberry, J. A., Rennolds, J., Clancy, J. P., Benos, D. J., Boyaka, P. N., & Sorscher, E. J. (2009) · The FASEB Journal · doi:10.1096/fj.08-127878 · Cited by 14 · see citing works
WS15.5 Transcomplementation by a truncation mutant of CFTR, Δ27-264 CFTR, rescues both trafficking and chloride channel function of ΔF508 CFTR
Cebotaru, L., Woodward, O. M., & Guggino, W. B. (2012) · Journal of Cystic Fibrosis · doi:10.1016/s1569-1993(12)60107-6
Self-citation
Rescuing cystic fibrosis transmembrane conductance regulator (CFTR)-processing mutants by transcomplementation
Cormet‐Boyaka, E., Jablonsky, M. J., Naren, A. P., Jackson, P. L., Muccio, D. D., & Kirk, K. L. (2004) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0400459101 · Cited by 66 · see citing works

Authors: Bergbower, E. A. S., Sabirzhanova, I. B., Boinot, C., Guggino, W. B., & Cebotaru, L.
Affiliations: Johns Hopkins University (US)
Corresponding author: Liudmila Cebotaru
ORCID: Emily Anne Smith Bergbower
William B. Guggino
Liudmila Cebotaru
Venue: Cellular Physiology and Biochemistry
Publisher: Cell Physiol Biochem Press GmbH and Co KG
Published: 2019-04-27
Volume: 52
Issue: 6
Pages: 1267-1279
ISSN: 1015-8987 (ISSN-L)
1421-9778
DOI: 10.33594/000000089
PMC: PMC7097968
OpenAlex: W2962756090
Cited by: 5
References: 39
Citations by year: 2025: 2 · 2024: 1 · 2021: 1 · 2019: 1
FWCI: 0.37
Type: journal article
Language: en
Open access: gold
doi.org
Licence: cc-by
Locations: Cellular Physiology and Biochemistry (publishedVersion, cc-by)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders: Cystic Fibrosis Foundation (GUGGIN14XX0)
National Institutes of Health
National Heart, Lung, and Blood Institute (R01HL122267, HL122267, F32HL103137)
Topics: Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Cystic Fibrosis Research Advances
Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Virus-based gene therapy research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA Interference and Gene Delivery
Keywords: cystic fibrosis, CFTR, F508del mutation, trans-complementation, adeno-associated virus gene therapy, endoplasmic reticulum, bimolecular interactions, airway epithelial cells, CFBE41o- cells, short-circuit current, plasma membrane trafficking, gene therapy
MeSH terms: Dependovirus, Cell Line, Cystic Fibrosis, Endoplasmic Reticulum, Humans, Transfection, Genetic Therapy, Sequence Deletion, Cystic Fibrosis Transmembrane Conductance Regulator, Respiratory Mucosa

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Restoration of F508-del Function by Transcomplementation: The Partners Meet in the Endoplasmic Reticulum

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