Revisiting the tubulin folding pathway: new roles in centrosomes and cilia

Gonçalves, João; Tavares, Alexandra; Carvalhal, Sara; Soares, Helena

doi:10.1515/bmc.2010.033

Cited by 11 publications

(8 citation statements)

References 124 publications

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“…2002; De Anda et al 2005) and cilia assembly (Gonçalves et al . 2010 b ). Having this in mind, we hypothesized that B. besnoiti and T. gondii may differentially explore this intrinsic polarity axis during host invasion, PV establishment and parasite replication.…”

Section: Discussionmentioning

confidence: 99%

Besnoitia besnoitiandToxoplasma gondii: two apicomplexan strategies to manipulate the host cell centrosome and Golgi apparatus

et al. 2014

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Besnoitia besnoiti and Toxoplasma gondii are two closely related parasites that interact with the host cell microtubule cytoskeleton during host cell invasion. Here we studied the relationship between the ability of these parasites to invade and to recruit the host cell centrosome and the Golgi apparatus. We observed that T. gondii recruits the host cell centrosome towards the parasitophorous vacuole (PV), whereas B. besnoiti does not. Notably, both parasites recruit the host Golgi apparatus to the PV but its organization is affected in different ways. We also investigated the impact of depleting and over-expressing the host centrosomal protein TBCCD1, involved in centrosome positioning and Golgi apparatus integrity, on the ability of these parasites to invade and replicate. Toxoplasma gondii replication rate decreases in cells over-expressing TBCCD1 but not in TBCCD1-depleted cells; while for B. besnoiti no differences were found. However, B. besnoiti promotes a reorganization of the Golgi ribbon previously fragmented by TBCCD1 depletion. These results suggest that successful establishment of PVs in the host cell requires modulation of the Golgi apparatus which probably involves modifications in microtubule cytoskeleton organization and dynamics. These differences in how T. gondii and B. besnoiti interact with their host cells may indicate different evolutionary paths.

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Section: Discussionmentioning

confidence: 99%

Besnoitia besnoitiandToxoplasma gondii: two apicomplexan strategies to manipulate the host cell centrosome and Golgi apparatus

et al. 2014

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“…CCT is a molecular chaperone involved in the folding of tubulin, actin and hundreds of other proteins. CCT subunits were also proposed 8 to have roles outside the chaperonin complex, and some localize at centrosomes and cilia (Goncalves et al, 2010;Seixas et al, 2003;Seixas et al, 2010;Sinha et al, 2014) where they may play roles related to the MT and actin-related processes of ciliogenesis. Myosin subunits were also identified, some of which (MYL12A/B, MYL3 or MYL6/B) only in serum-starved cells.…”

Section: Resultsmentioning

confidence: 99%

LUZP1 and the tumour suppressor EPLIN are negative regulators of primary cilia formation

Gonçalves

Coyaud

Laurent

et al. 2019

Preprint

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Running title: LUZP1 and EPLIN regulate ciliogenesis SUMMARY Gonçalves et al. show that LUZP1 and its interactor EPLIN are negative regulators of ciliogenesis. LUZP1 is a novel actin-stabilizing protein localizing at the centrosome and basal body where it may regulate actin-associated processes. 2 ABSTRACT Cilia/flagella are microtubule-based cellular projections with important sensory and motility functions. Their absence or malfunction is associated with a growing number of human diseases collectively referred to as ciliopathies. However, the fundamental mechanisms underpinning cilia biogenesis and functions remain only partly understood. Here, we show that LUZP1, and its interacting protein EPLIN, are negative regulators of primary cilia formation. LUZP1 is an actinassociated protein that localizes to both actin filaments and the centrosome/basal body. Like EPLIN, LUZP1 is an actin-stabilizing protein and likely regulates actin dynamics at the centrosome. Both proteins interact with ciliogenesis and cilia length regulators, and are potential players in the actin-dependent processes involved in centrosome to basal body conversion. Ciliogenesis deregulation caused by LUZP1 or EPLIN loss may contribute to the pathology of their associated diseases.

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“…Our data therefore indicate that rp2 mRNA from maternal origin allows the expression of the Rp2 protein before the onset of epiboly and clearly suggest a role of Rp2 in embryonic development from the beginning of the gastrulation process. As Rp2 partially overlaps with Tubulin Binding Cofactor C (TBCC) protein function [8], it has been suggested to contribute to cell cycle progression through microtubule polymerization/nucleation in cell centrioles [42]. The role of Rp2 in the gastrulation process has however not been studied so far and deserves further attention.…”

Section: Oocyte-specific Rp2 Mrna Is Maternally-inherited In the Zebrafish Eggmentioning

confidence: 99%

X-Linked Retinitis Pigmentosa 2 Is a Novel Maternal-Effect Gene Required for Left-Right Asymmetry in Zebrafish1

Desvignes

Nguyen

Chesnel

et al. 2015

Biology of Reproduction

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Retinitis pigmentosa 2 (RP2) gene is responsible for up to 20% of X-linked retinitis pigmentosa, a severe heterogeneous genetic disorder resulting in progressive retinal degeneration in humans. In vertebrates, several bodies of evidence have clearly established the role of Rp2 protein in cilia genesis and/or function. Unexpectedly, some observations in zebrafish have suggested the oocyte-predominant expression of the rp2 gene, a typical feature of maternal-effect genes. In the present study, we investigate the maternal inheritance of rp2 gene products in zebrafish eggs in order to address whether rp2 could be a novel maternal-effect gene required for normal development. Although both rp2 mRNA and corresponding protein are expressed during oogenesis, rp2 mRNA is maternally inherited, in contrast to Rp2 protein. A knockdown of the protein transcribed from both rp2 maternal and zygotic mRNA results in delayed epiboly and severe developmental defects, including eye malformations, that were not observed when only the protein from zygotic origin was knocked down. Moreover, the knockdown of maternal and zygotic Rp2 revealed a high incidence of left-right asymmetry establishment defects compared to only zygotic knockdown. Here we show that rp2 is a novel maternal-effect gene exclusively expressed in oocytes within the zebrafish ovary and demonstrate that maternal rp2 mRNA is essential for successful embryonic development and thus contributes to egg developmental competence. Our observations also reveal that Rp2 protein translated from maternal mRNA is important to allow normal heart loop formation, thus providing evidence of a direct maternal contribution to left-right asymmetry establishment.

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Revisiting the tubulin folding pathway: new roles in centrosomes and cilia

Cited by 11 publications

References 124 publications

Besnoitia besnoitiandToxoplasma gondii: two apicomplexan strategies to manipulate the host cell centrosome and Golgi apparatus

Besnoitia besnoitiandToxoplasma gondii: two apicomplexan strategies to manipulate the host cell centrosome and Golgi apparatus

LUZP1 and the tumour suppressor EPLIN are negative regulators of primary cilia formation

X-Linked Retinitis Pigmentosa 2 Is a Novel Maternal-Effect Gene Required for Left-Right Asymmetry in Zebrafish1

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