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ER-associated retrograde SNAREs and the Dsl1 complex mediate an alternative, Sey1p-independent homotypic ER fusion pathway.

Rogers JV, McMahon C, Baryshnikova A, Hughson FM, Rose MD - Mol. Biol. Cell (2014)

Bottom Line: However, an alternative explanation--that the observed phenotypes arose from perturbed vesicle trafficking--could not be ruled out.In contrast, cytosolic coat protein I (COPI) vesicle coat mutations in sey1Δ cells caused no synthetic defects, excluding perturbed retrograde trafficking as a cause for the previously observed synthetic defects.We conclude that the ER SNAREs and the Dsl1 complex directly mediate Sey1p-independent ER-ER fusion and that, in the absence of both pathways, cell viability depends upon membrane curvature-promoting reticulons.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Biology, Princeton University, Princeton, NJ 08544-1014.

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Mentions: It remained possible that the synthetic growth defects observed in sey1Δ dsl1ΔE double mutants were due to disruption of some other process required for normal growth, other than ER–ER fusion or vesicle trafficking. We therefore examined these mutants for ER structure defects that should arise from disrupted homotypic ER fusion. In wild-type cells, Sec63-GFP marks the entire ER network, which includes the nucleus, tubules extending from the nucleus to the cell cortex, and the tubules and sheets at the cell periphery. Sec63–green fluorescent protein (GFP) distribution appeared similar to wild type in sey1Δ and dsl1ΔE single mutants, but sey1Δ dsl1ΔE double mutants exhibited severely disrupted peripheral ER, lacking an organized tubular network and mostly appearing as patches or aggregates of peripheral ER (Figure 4A). The pool of ER near the plasma membrane is consistent with an inability for growing ER tubules to fuse at other parts of the ER network. Additionally, whereas in wild-type cells the ER forms an almost continuous network close to the plasma membrane, in sey1Δ dsl1ΔE mutant cells, we frequently observed large sections of the cortex with no ER and regions of ER internal to the cell.


ER-associated retrograde SNAREs and the Dsl1 complex mediate an alternative, Sey1p-independent homotypic ER fusion pathway.

Rogers JV, McMahon C, Baryshnikova A, Hughson FM, Rose MD - Mol. Biol. Cell (2014)

© Copyright Policy - creative-commons
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4214786&req=5

Mentions: It remained possible that the synthetic growth defects observed in sey1Δ dsl1ΔE double mutants were due to disruption of some other process required for normal growth, other than ER–ER fusion or vesicle trafficking. We therefore examined these mutants for ER structure defects that should arise from disrupted homotypic ER fusion. In wild-type cells, Sec63-GFP marks the entire ER network, which includes the nucleus, tubules extending from the nucleus to the cell cortex, and the tubules and sheets at the cell periphery. Sec63–green fluorescent protein (GFP) distribution appeared similar to wild type in sey1Δ and dsl1ΔE single mutants, but sey1Δ dsl1ΔE double mutants exhibited severely disrupted peripheral ER, lacking an organized tubular network and mostly appearing as patches or aggregates of peripheral ER (Figure 4A). The pool of ER near the plasma membrane is consistent with an inability for growing ER tubules to fuse at other parts of the ER network. Additionally, whereas in wild-type cells the ER forms an almost continuous network close to the plasma membrane, in sey1Δ dsl1ΔE mutant cells, we frequently observed large sections of the cortex with no ER and regions of ER internal to the cell.

Bottom Line: However, an alternative explanation--that the observed phenotypes arose from perturbed vesicle trafficking--could not be ruled out.In contrast, cytosolic coat protein I (COPI) vesicle coat mutations in sey1Δ cells caused no synthetic defects, excluding perturbed retrograde trafficking as a cause for the previously observed synthetic defects.We conclude that the ER SNAREs and the Dsl1 complex directly mediate Sey1p-independent ER-ER fusion and that, in the absence of both pathways, cell viability depends upon membrane curvature-promoting reticulons.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Biology, Princeton University, Princeton, NJ 08544-1014.

Show MeSH
Related in: MedlinePlus