Organelle Membrane Fusion: A Novel Function for the Syntaxin Homolog Ufe1p in ER Membrane Fusion

Patel, Sheetal; Indig, Fred E.; Olivieri, Nicoletta; Levine, Nicole D; Latterich, Martin

doi:10.1016/s0092-8674(00)81129-0

Cited by 149 publications

(142 citation statements)

References 33 publications

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“…55 Interestingly, p31 and RINT1 are forming the 'Syntaxin 18 SNARE' complex together with Syntaxin 18, BNIP1, Sec22B, Sly1p, NAG and ZW10. 10,11 'Syntaxin 18 SNARE' complex was found to be implicated in membrane fusion of retrograde transport 10,56,57 while its members Sec22B and ZW10/RINT1 are also involved in the anterograde transport. 16,58 RINT1 was shown to be also involved in the more specific Rab6-dependent recycling pathway from the Golgi to the ER.…”

Section: Discussionmentioning

confidence: 99%

Rint1 inactivation triggers genomic instability, ER stress and autophagy inhibition in the brain

et al. 2015

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Endoplasmic reticulum (ER) stress, defective autophagy and genomic instability in the central nervous system are often associated with severe developmental defects and neurodegeneration. Here, we reveal the role played by Rint1 in these different biological pathways to ensure normal development of the central nervous system and to prevent neurodegeneration. We found that inactivation of Rint1 in neuroprogenitors led to death at birth. Depletion of Rint1 caused genomic instability due to chromosome fusion in dividing cells. Furthermore, Rint1 deletion in developing brain promotes the disruption of ER and Cis/Trans Golgi homeostasis in neurons, followed by ER-stress increase. Interestingly, Rint1 deficiency was also associated with the inhibition of the autophagosome clearance. Altogether, our findings highlight the crucial roles of Rint1 in vivo in genomic stability maintenance, as well as in prevention of ER stress and autophagy.

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Section: Discussionmentioning

confidence: 99%

Rint1 inactivation triggers genomic instability, ER stress and autophagy inhibition in the brain

et al. 2015

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“…At the same time, the mammalian orthologue of Cdc48, p97, was shown to be involved in the reconstitution of Golgi cisternae from mitotic Golgi fragments [13]. Later, evidence was presented that Cdc48 works in conjunction with the ER-localized target-soluble NSF attachment protein (SNAP) receptor (t-SNARE) Ufe1p [14]. Subsequent work has confirmed the role of p97 in the dynamics of ER architecture [15,16], but also indicates the participation of additional mechanisms.…”

Section: Homotypic Fusionmentioning

confidence: 98%

Endoplasmic reticulum architecture: structures in flux

Borgese

Francolini

Snapp

2006

Current Opinion in Cell Biology

196

147

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The endoplasmic reticulum (ER) is a dynamic pleiomorphic organelle containing continuous but distinct subdomains. The diversity of ER structures parallels its many functions, including secretory protein biogenesis, lipid synthesis, drug metabolism and Ca 2+ signaling. Recent studies are revealing how elaborate ER structures arise in response to subtle changes in protein levels, dynamics, and interactions as well as in response to alterations in cytosolic ion concentrations. Subdomain formation appears to be governed by principles of self-organization. Once formed, ER subdomains remain malleable and can be rapidly transformed into alternative structures in response to altered conditions. The mechanisms that modulate ER structure are likely to be important for the generation of the characteristic shapes of other organelles.

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“…Under these conditions, secretion of invertase is blocked, but the desaturase is still observed to relocalize, indicating that relocalization is not energy dependent (unpublished data). To examine whether formation of the peripheral desaturase-containing structures requires SNARE function, relocalization of the desaturase was analyzed in ts mutants of UFE1 and SED5, two syntaxin homologues required for ER (Lewis and Pelham, 1996;Patel et al, 1998) and Golgi fusion (Hardwick and Pelham, 1992), respectively. This analysis revealed that UFE1 but not SED5 was required for the formation of the peripheral membrane compartment, indicating that the peripheral compartment is an ER derivative ( Figure 11).…”

Section: Formation Of the Peripheral Desaturase-enriched Compartment mentioning

confidence: 99%

Lipid-dependent Subcellular Relocalization of the Acyl Chain Desaturase in Yeast

Tatzer¹,

Zellnig

Kohlwein

et al. 2002

MBoC

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The degree of acyl chain desaturation of membrane lipids is a critical determinant of membrane fluidity. Temperature-sensitive mutants of the single essential acyl chain desaturase, Ole1p, of yeast have previously been isolated in screens for mitochondrial inheritance mutants (Stewart, L.C., and Yaffe, M.P. ). J. Cell Biol. 115, 1249 -1257. We now report that the mutant desaturase relocalizes from its uniform ER distribution to a more punctuate localization at the cell periphery upon inactivation of the enzyme. This relocalization takes place within minutes at nonpermissive conditions, a time scale at which mitochondrial morphology and inheritance is not yet affected. Relocalization of the desaturase is fully reversible and does not affect the steady state localization of other ER resident proteins or the kinetic and fidelity of the secretory pathway, indicating a high degree of selectivity for the desaturase. Relocalization of the desaturase is energy independent but is lipid dependent because it is rescued by supplementation with unsaturated fatty acids. Relocalization of the desaturase is also observed in cells treated with inhibitors of the enzyme, indicating that it is independent of temperature-induced alterations of the enzyme. In the absence of desaturase function, lipid synthesis continues, resulting in the generation of lipids with saturated acyl chains. A model is discussed in which the accumulation of saturated lipids in a microdomain around the desaturase could induce the observed segregation and relocalization of the enzyme.

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Organelle Membrane Fusion: A Novel Function for the Syntaxin Homolog Ufe1p in ER Membrane Fusion

Cited by 149 publications

References 33 publications

Rint1 inactivation triggers genomic instability, ER stress and autophagy inhibition in the brain

Rint1 inactivation triggers genomic instability, ER stress and autophagy inhibition in the brain

Endoplasmic reticulum architecture: structures in flux

Lipid-dependent Subcellular Relocalization of the Acyl Chain Desaturase in Yeast

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