Distinct Functions for Arf Guanine Nucleotide Exchange Factors at the Golgi Complex: GBF1 and BIGs Are Required for Assembly and Maintenance of the Golgi Stack and<i>trans</i>-Golgi Network, Respectively

Manolea, Florin; Claude, Alejandro; Chun, Justin; Castro-Rosas, Javier; Melançon, Paul

doi:10.1091/mbc.e07-04-0394

Cited by 97 publications

(133 citation statements)

References 86 publications

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“…We could demonstrate that BFA can partially resemble the phenotype of Arfgef2 GT/GT mutant embryonic development. One can argue that BFA inhibits not only BIG2 but also GBF1 and BIG1, however, it has been demonstrated that overexpression of GBF1 and BIGs have opposite effects on the sensitivity to BFA (Claude et al 1999;Shinotsuka et al 2002b;Manolea et al 2008). Moreover, the phenotype of GBF1-depleted cells by using siRNA differed significantly from those observed in cells incubated with BFA (Szul et al 2007).…”

Section: Discussionmentioning

confidence: 99%

Early embryonic lethality in gene trap mice with disruption of the Arfgef2 gene

Grzmil

Enkhbaatar²,

Gundsambuu³

et al. 2010

Int. J. Dev. Biol.

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The switching of ADP-ribosylation factors from the inactive form to the active form is catalyzed by ARF-GEF (ADP ribosylation factor -guanine nucleotide exchange protein) proteins containing a Sec7 domain. The murine Arfgef2 gene encoding the BIG2 protein belongs to the class of high molecular mass (>100 kDa) ARF-GEF proteins. BIG2 is believed to be associated with the trans-Golgi network and the recycling endosomes. In humans, mutations in the ARFGEF2 gene cause autosomal recessive periventricular heterotopia with microcephaly. To elucidate the function of BIG2 in mouse we studied a gene-trap mouse line with a functional disruption of the Arfgef2 gene. Heterozygous mutants did not reveal phenotypic abnormalities and were fertile. However, no homozygous embryos were obtained from breeding heterozygous females and males. To explore the reason for embryonic lethality, we analysed the pattern of expression of Arfgef2. Arfgef2 transcripts were detected in several adult tissues. Interestingly, Arfgef2 undergoes alternative splicing and the splicing pattern differs among tissues from adult animals. Moreover, the LacZ reporter gene of the gene-trap construct was used to reveal the expression of Arfgef2 during embryonic development. Here, we show that Arfgef2 mRNA is stored in the oocyte and is likely translated during the first embryonic divisions. SNP (Single Nucleotide Polymorphism) markers were used to demonstrate that the embryonic Arfgef2 gene is activated first at the 4-cell stage, suggesting an important role for embryonic development. This assumption is supported by the failure of Arfgef2-deficient oocytes fertilized with Arfgef2-deficient sperm to develop into 4-cell stage embryos. Our results indicate that murine BIG2 is essential for early embryonic development.

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Section: Discussionmentioning

confidence: 99%

Early embryonic lethality in gene trap mice with disruption of the Arfgef2 gene

Grzmil

Enkhbaatar²,

Gundsambuu³

et al. 2010

Int. J. Dev. Biol.

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“…The heptameric COPI complex associates with the Golgi membranes, resulting in the budding of COPI-containing vesicles, whose major function is to mediate transport of cellular proteins and cargo from the Golgi to the ER as well as the intra-Golgi transport (20). Depletion of COPI also perturbs the steady-state distribution of the Golgi enzymes (43) and thus inhibits processing of the VSV G protein and its transport to the plasma membrane (44,45). Further, we have found that depletion of COPZ1 subunit had no adverse effect on VSV G protein-mediated entry of pseudotyped HIV (Fig.…”

Section: Discussionmentioning

confidence: 99%

RNAi screening reveals requirement for host cell secretory pathway in infection by diverse families of negative-strand RNA viruses

Panda

Das

Dinh

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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Negative-strand (NS) RNA viruses comprise many pathogens that cause serious diseases in humans and animals. Despite their clinical importance, little is known about the host factors required for their infection. Using vesicular stomatitis virus (VSV), a prototypic NS RNA virus in the family Rhabdoviridae, we conducted a human genomewide siRNA screen and identified 72 host genes required for viral infection. Many of these identified genes were also required for infection by two other NS RNA viruses, the lymphocytic choriomeningitis virus of the Arenaviridae family and human parainfluenza virus type 3 of the Paramyxoviridae family. Genes affecting different stages of VSV infection, such as entry/uncoating, gene expression, and assembly/release, were identified. Depletion of the proteins of the coatomer complex I or its upstream effectors ARF1 or GBF1 led to detection of reduced levels of VSV RNA. Coatomer complex I was also required for infection of lymphocytic choriomeningitis virus and human parainfluenza virus type 3. These results highlight the evolutionarily conserved requirements for gene expression of diverse families of NS RNA viruses and demonstrate the involvement of host cell secretory pathway in the process.RNA interference | transcription and replication | host cell factors for virus infection

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“…GBF1 is critical for biogenesis of the Golgi ribbon in mammalian cells 10,13,25,[54][55][56] and for recruitment of the COPI coat that mediates protein traffic at the ER-Golgi interface and of the AP-1 and GGA adaptors that function at the TGN. 10,11,13,25,57 The architecture of the Golgi differs in mammalian and Drosophila cells and the Golgi ribbon found in mammalian cells is replaced by scattered but still polarized Golgi mini-stacks in Drosophila cells.…”

Section: Discussionmentioning

confidence: 99%