Embryonic Lethality Caused by Apoptosis during Gastrulation in Mice Lacking the Gene of the ADP-Ribosylation Factor-Related Protein 1

Mueller, A.G.; Moser, Markus; Kluge, Reinhart; Leder, Susanne; Blum, Martin; Büttner, R.; Joost, Hans‐Georg; Schürmann, Annette

doi:10.1128/mcb.22.5.1488-1494.2002

Cited by 50 publications

(35 citation statements)

References 31 publications

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“…This may reflect a nonspecific response, since a number of knockout mice show this effect (28). Alternatively, Miz1 might be involved in a survival pathway that relays adhesion-dependent survival signals to ectodermal cells.…”

Section: Discussionmentioning

confidence: 99%

Miz1 Is Required for Early Embryonic Development during Gastrulation

Adhikary¹,

Peukert²,

Karsunky

et al. 2003

Molecular and Cellular Biology

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Miz1 is a member of the POZ domain/zinc finger transcription factor family. In vivo, Miz1 forms a complex with the Myc oncoprotein and recruits Myc to core promoter elements. The MYC (or c-MYC) gene and two of its relatives, MYCL and MYCN, are causally involved in the genesis of a wide variety of human tumors (32). c-MYC encodes a transcription factor (Myc) that can both activate and repress transcription. Myc activates transcription as part of a heterodimeric complex with the Max protein (1, 23). The complex binds to specific sequences, termed E-boxes, and recruits both the Gcn5 and Tip60 histone acetylase complexes to E-box elements through interaction with the TRRAP protein (8,16,17,25,26). In addition, TRRAP-independent mechanisms of transcriptional activation have been demonstrated (30). These may involve interactions of Myc with the P-TEFb complex, which regulates transcriptional elongation (14). Both directed searches and a number of array analyses have identified a large number of genes that are activated by Myc in vivo (9,27,31,45).Similarly, a large number of genes have been identified that are repressed upon activation of Myc. However, the mechanisms of transcriptional repression by Myc have remained more elusive. For a number of genes, repression of Myc has been mapped to the core promoter, suggesting that Myc affects proteins that regulate transcription at or close to the start site of transcription (24). One suggestion has been that Myc directs the synthesis of a transcriptional repressor protein and thereby indirectly represses transcription, but such a repressor has not yet been identified. A second suggestion has been that MycMax complexes directly bind to the start site of one repressed gene, p27kip1 (49), but direct binding of Myc-Max complexes to start sites of other repressed genes has not been found. A third suggestion, therefore, has been that Myc is recruited to core promoters through protein-protein interactions with other transcription factors. A number of candidate interaction partners have been identified, including TFII-I (35), YY-1 (38), Smad2 (15), Sp1 (18), and Miz1 (34).Recently, evidence has accumulated that three genes, p15Ink4b (37, 40), p21Cip1 (20,36,43,48), and Mad4 (22), are repressed by Myc through interaction with Miz1. Miz1 is a transcription factor with 13 zinc fingers and a POZ/BTB domain at its amino terminus (4). Free Miz1 binds to the core promoter of all three genes and activates transcription. Upon binding to Myc, transcriptional activation by Miz1 is abolished, and the Myc-Miz1 complex acts as a transcriptional repressor; this is in part due to competition between p300 and Myc for binding to Miz1 (40). Array analyses and chromatin immunoprecipitation (ChIp) experiments suggest that several other genes that are repressed by Myc, including p57Kip2 (12) and C/EBP␣ (24), are directly repressed by Myc through interaction with Miz1 (V. Beuger and M. Eilers, unpublished observations).These findings suggest that interaction with Miz1 plays a central role in transcriptio...

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Section: Discussionmentioning

confidence: 99%

Miz1 Is Required for Early Embryonic Development during Gastrulation

Adhikary¹,

Peukert²,

Karsunky

et al. 2003

Molecular and Cellular Biology

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“…The functional importance of ARFRP1 is underscored by the finding that targeted disruption of the Arfrp1 gene in mice resulted in embryonic lethality at the gastrulation stage and apoptosis of ectodermal cells (Mueller et al, 2002). Studies in yeast have shown that Arl3p is required for recruitment of Arl1p and the GRIP domain-containing protein, Imh1p/Sys3p, onto the Golgi (Gangi Setty et al, 2003;Panic et al, 2003b).…”

Section: Introductionmentioning

confidence: 99%

Roles of ARFRP1 (ADP-ribosylation factor-related protein 1) in post-Golgi membrane trafficking

Shin

Kobayashi

Kitamura

et al. 2005

Journal of Cell Science

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ADP-ribosylation factor (ARF)-related protein 1 (ARFRP1) is a small GTPase with significant similarity to the ARF family. However, little is known about the function of ARFRP1 in mammalian cells, although knockout mice of its gene are embryonic lethal. In the present study, we demonstrate that ARFRP1 is associated mainly with the trans-Golgi compartment and the trans-Golgi network (TGN) and is an essential regulatory factor for targeting of Arl1 and GRIP domain-containing proteins, golgin-97 and golgin-245, onto Golgi membranes. Furthermore, we show that, in concert with Arl1 and GRIP proteins, ARFRP1 is implicated in the Golgi-to-plasma membrane transport of the vesicular stomatitis virus G protein as well as in the retrograde transport of TGN38 and Shiga toxin from endosomes to the TGN.Supplementary material available online at

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“…Rounded pyknotic cells within this area were only loosely attached to the ectodermal cell layer, and some apoptotic cells were found in the proamniotic cavity. This observation suggested that ARFRP1 plays a critical role in processes during early gastrulation such as adhesion-dependent morphogenesis, cytoskeletal reorganization, and/or development of cell polarity (11).…”

mentioning

confidence: 99%

“…Deletion of Arfrp1 in mice resulted in embryonic lethality (11). Arfrp1 Ϫ/Ϫ blastocysts implanted in vivo and formed egg cylinder-stage embryos that appeared normal until day 5.…”

mentioning

confidence: 99%

ADP-ribosylation Factor-like GTPase ARFRP1 Is Required for Trans-Golgi to Plasma Membrane Trafficking of E-cadherin

Zahn

Jaschke

Weiske

et al. 2008

Journal of Biological Chemistry

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ADP-ribosylation factor-related protein 1 (ARFRP1) plays a specific role in Golgi function controlling recruitment of GRIP domain proteins and ARL1 to the trans-Golgi. Deletion of the mouse Arfrp1 gene causes embryonic lethality during early gastrulation, because epiblast cells detach from the ectodermal cell layer and do not differentiate to mesodermal tissue. Here we show that in Arfrp1 ؊/؊ embryos E-cadherin is mistargeted to intracellular compartments, whereas in control embryos it is present at the cell surface of trophectodermal and ectodermal cells. In enterocytes of intestine-specific Arfrp1 null mutants (Arfrp1), E-cadherin is associated with intracellular membranes, partially colocalizing with the cis-Golgi marker GM130 or with punctae close to the cell surface. In contrast, in control enterocytes E-cadherin is exclusively located in the lateral membranes. In addition, ARL1 is dislocated from Golgi membranes to the cytosol of Arfrp1 vil؊/؊ enterocytes. Depletion of endogenous ARFRP1 by RNA interference leads to a dislocation of E-cadherin from the cell surface in HeLa cells and to a reduced cell aggregation in Ltk ؊ Ecad cells. ARFRP1 was coimmunoprecipitated in a complex with E-cadherin, ␣-catenin, ␤-catenin, ␥-catenin, and p120 ctn from lysates of MadinDarby canine kidney cells stably expressing myc-ARFRP1. These data indicate that knock-out of Arfrp1 disrupts the trafficking of E-cadherin through the Golgi and suggest an essential role of the GTPase in trans-Golgi network function.

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Embryonic Lethality Caused by Apoptosis during Gastrulation in Mice Lacking the Gene of the ADP-Ribosylation Factor-Related Protein 1

Cited by 50 publications

References 31 publications

Miz1 Is Required for Early Embryonic Development during Gastrulation

Miz1 Is Required for Early Embryonic Development during Gastrulation

Roles of ARFRP1 (ADP-ribosylation factor-related protein 1) in post-Golgi membrane trafficking

ADP-ribosylation Factor-like GTPase ARFRP1 Is Required for Trans-Golgi to Plasma Membrane Trafficking of E-cadherin

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