June 2023
Volume 64, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2023
Lysine 63-linked ubiquitin chains mark mistargeted proteins for removal from the photoreceptor outer segment
Author Affiliations & Notes
  • Tirthasree Das
    Ophthalmology, University of California San Francisco, San Francisco, California, United States
  • Gary Andrew Bradshaw
    Harvard Program in Therapeutic Science, Harvard Medical School, Boston, Massachusetts, United States
  • Robyn Eisert
    Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts, United States
  • Yien Ming Kuo
    Ophthalmology, University of California San Francisco, San Francisco, California, United States
  • Marian Kalocsay
    The University of Texas MD Anderson Cancer Center Division of Radiation Oncology, Houston, Texas, United States
  • Maxence Nachury
    Ophthalmology, University of California San Francisco, San Francisco, California, United States
  • Footnotes
    Commercial Relationships   Tirthasree Das None; Gary Bradshaw None; Robyn Eisert None; Yien Ming Kuo None; Marian Kalocsay None; Maxence Nachury None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science June 2023, Vol.64, 3898. doi:
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      Tirthasree Das, Gary Andrew Bradshaw, Robyn Eisert, Yien Ming Kuo, Marian Kalocsay, Maxence Nachury; Lysine 63-linked ubiquitin chains mark mistargeted proteins for removal from the photoreceptor outer segment. Invest. Ophthalmol. Vis. Sci. 2023;64(8):3898.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose : The accumulation of non-resident proteins in the outer segment (OS) of photoreceptors is a hallmark of the genetic disorder Bardet-Biedl Syndrome (BBS) and may underlie retinal degeneration in BBS. The BBSome is a complex of eight BBS proteins that ferries membrane proteins out of cilia, the equivalent of the OS in photoreceptors. Prior work in cultured cells demonstrated that lysine 63-linked ubiquitin (Ub) chains mark dynamic BBSome cargoes for their removal from primary cilia. In this study, we sought to test whether UbK63 chains mark mistargeted proteins for removal from the OS by the BBSome.

Methods : To determine whether ubiquitin and specific Ub linkages accumulate in OS when BBSome function is compromised, we imaged Ub and Ub linkages in retinal sections of Bbs4-/- mice at developmental stages preceding retinal degeneration. We next isolated UbK63-associated proteins from Bbs4-/- OS using engineered affinity reagents and inventoried the corresponding proteome by quantitative mass spectrometry. To validate the ubiquitination profile of the proteins accumulating in Bbs OS, we biochemically isolated the covalently ubiquitinated proteins from Bbs4-/- OS under denaturating conditions.

Results : We found that the levels of Ub and UbK63 linkage increase 3- and 2-fold in Bbs4-/- OS respectively compared to controls. The UbK63-associated proteome of Bbs4-/- OS revealed 49 proteins enriched (p < 0.05) by >1.5-fold compared to wildtype. The vast majority of these proteins are membrane proteins that are known to localize to the inner segment, to synaptic vesicles, or to the synaptic terminal. By biochemically isolating ubiquitinated proteins under denaturing conditions, we validated 2 proteins that are differentially ubiquitinated in Bbs4-/- OS compared to wildtype OS. Immunofluorescence imaging further revealed that these validated ubiquitinated non-OS proteins accumulate in Bbs4-/- OS starting at the earliest stages of outer segment morphogenesis.

Conclusions : We identify several novel cargoes of the BBSome in photoreceptors and demonstrate that UbK63 chains mark these mistargeted cargoes for removal from the OS as they do for removal from cilia for dynamic cargoes. We propose that non-resident proteins are recognized as foreign material by the ubiquitination machinery in the OS before clearance by the BBSome.

This abstract was presented at the 2023 ARVO Annual Meeting, held in New Orleans, LA, April 23-27, 2023.

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