Researcher:
Culfa, Efraim

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Master Student

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Efraim

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Culfa

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Culfa, Efraim

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2016 - 20204

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Researcher Of Publications: search.filters.isAuthorOfPublication.f3e0ed11-1d25-48dc-aa03-e270a9d8834c

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    The centrosome protein CEP103 binds to microtubules and is required for efficient ciliogenesis
    (amer Soc Cell biology, 2018) N/A; N/A; Culfa, Efraim; N/A; Master Student; N/A; Graduate School of Sciences and Engineering; N/A; N/A
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    The centriolar satellite protein Cep109 and Cep290 interact and are required for recruitment of BBS proteins to the cilium
    (Amer Soc Cell Biology, 2016) Rauniyar, N.; Yates, J., I. I. I.; N/A; N/A; N/A; Department of Molecular Biology and Genetics; Çonkar, Deniz; Culfa, Efraim; Odabaşı, Ezgi; Karalar, Elif Nur Fırat; Phd Student; Master Student; Other; Faculty Member; Department of Molecular Biology and Genetics; Graduate School of Sciences and Engineering; N/A; N/A; College of Sciences; N/A; N/A; N/A; 206349
    Defects in centrosome and cilium function are associated with phenotypically related syndromes called ciliopathies. Centriolar satellites are centrosome-associated structures, defined by the protein PCM1, that are implicated in centrosomal protein trafficking. We identify Cep72 as a PCM1-interacting protein required for recruitment of the ciliopathy-associated protein Cep290 to centriolar satellites. Loss of centriolar satellites by depletion of PCM1 causes relocalization of Cep72 and Cep290 from satellites to the centrosome, suggesting that their association with centriolar satellites normally restricts their centrosomal localization. We identify interactions between PCM1, Cep72, and Cep290 and find that disruption of centriolar satellites by overexpression of Cep72 results in specific aggregation of these proteins and the BBSome component BBS4. During ciliogenesis, BBS4 relocalizes from centriolar satellites to the primary cilium. This relocalization occurs normally in the absence of centriolar satellites (PCM1 depletion) but is impaired by depletion of Cep290 or Cep72, resulting in defective ciliary recruitment of the BBSome subunit BBS8. We propose that Cep290 and Cep72 in centriolar satellites regulate the ciliary localization of BBS4, which in turn affects assembly and recruitment of the BBSome. Finally, we show that loss of centriolar satellites in zebrafish leads to phenotypes consistent with cilium dysfunction and analogous to those observed in human ciliopathies.
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    PublicationOpen Access
    CCDC57 cooperates with microtubules and microcephaly protein CEP63 and regulates centriole duplication and mitotic progression
    (Elsevier, 2020) Lince Faria, Mariana; Department of Molecular Biology and Genetics; Gürkaşlar, Hazal Kübra; Culfa, Efraim; Arslanhan, Melis Dilara; Karalar, Elif Nur Fırat; Master Student; Department of Molecular Biology and Genetics; Graduate School of Sciences and Engineering; College of Sciences; N/A; N/A; N/A; 206349
    Centrosomes function in key cellular processes ranging from cell division to cellular signaling. Their dysfunction is linked to cancer and developmental disorders. Here, we identify CCDC57 as a pleiotropic regulator of centriole duplication, mitosis, and ciliogenesis. Combining proximity mapping with superresolution imaging, we show that CCDC57 localizes to the proximal end of centrioles and interacts with the microcephaly protein CEP63, centriolar satellite proteins, and microtubules. Loss of CCDC57 causes defects in centriole duplication and results in a failure to localize CEP63 and CEP152 to the centrosome. Additionally, CCDC57 depletion perturbs mitotic progression both in wild-type and centriole-less cells. Importantly, its centrosome-targeting region is required for its interaction with CEP63 and functions during centriole duplication and cilium assembly, whereas the microtubule-targeting region is required for its mitotic functions. Together, our results identify CCDC57 as a critical interface between centrosome and microtubule-mediated cellular processes that are deregulated in microcephaly.
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    PublicationOpen Access
    The centriolar satellite protein CCDC66 interacts with CEP290 and functions in cilium formation and trafficking
    (The Company of Biologists (United Kingdom), 2017) Rauniyar, Navin; Yates, John R., III; Department of Molecular Biology and Genetics; Karalar, Elif Nur Fırat; Çonkar, Deniz; Culfa, Efraim; Odabaşı, Ezgi; PhD Student; Master Student; Other; Department of Molecular Biology and Genetics; Graduate School of Sciences and Engineering; 206349; N/A; N/A; N/A
    Centriolar satellites are membrane-less structures that localize and move around the centrosome and cilium complex in a microtubule-dependent manner. They play important roles in centrosome- and cilium-related processes, including protein trafficking to the centrosome and cilium complex, and ciliogenesis, and they are implicated in ciliopathies. Despite the important regulatory roles of centriolar satellites in the assembly and function of the centrosome and cilium complex, the molecular mechanisms of their functions remain poorly understood. To dissect the mechanism for their regulatory roles during ciliogenesis, we performed an analysis to determine the proteins that localize in close proximity to the satellite protein CEP72, among which was the retinal degeneration gene product CCDC66. We identified CCDC66 as a microtubule-associated protein that dynamically localizes to the centrosome, centriolar satellites and the primary cilium throughout the cell cycle. Like the bbsome component BBS4, CCDC66 distributes between satellites and the primary cilium during ciliogenesis. CCDC66 has extensive proximity interactions with centrosome and centriolar satellite proteins, and co-immunoprecipitation experiments revealed interactions between CCDC66, CEP290 and PCM1. Ciliogenesis, ciliary recruitment of BBS4 and centriolar satellite organization are impaired in cells depleted for CCDC66. Taken together, our findings identify CCDC66 as a targeting factor for centrosome and cilium proteins.