2015
DOI: 10.1083/jcb.20101208307062015r
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Peroxisome reintroduction in Hansenula polymorpha requires Pex25 and Rho1

Abstract: The editors of The Journal of Cell Biology have been notified by Dr. Ida J. van der Klei that she and the other authors of the paper referenced above retract the paper. As a result of this retraction, no data in this paper should be cited in the scientific literature.

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Cited by 3 publications
(9 citation statements)
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“…In contrast, the phenotype of the corresponding double mutant is more severe with most cells being characterized by a greater reduction in peroxisome number when compared to the single deletion strains and a mislocalization of at least one peroxisomal matrix protein to the cytosol (Tower et al, 2011). Moreover, Pex25p has been reported to be required for the de novo -formation of peroxisomes (Huber et al, 2012, Saraya et al, 2011). To gain more insight into a putative concerted function of Pex34p and Pex25p, we first compared the phenotype of pex34 Δ pex25 Δ cells upon inducing and non-inducing conditions.…”
Section: Resultsmentioning
confidence: 99%
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“…In contrast, the phenotype of the corresponding double mutant is more severe with most cells being characterized by a greater reduction in peroxisome number when compared to the single deletion strains and a mislocalization of at least one peroxisomal matrix protein to the cytosol (Tower et al, 2011). Moreover, Pex25p has been reported to be required for the de novo -formation of peroxisomes (Huber et al, 2012, Saraya et al, 2011). To gain more insight into a putative concerted function of Pex34p and Pex25p, we first compared the phenotype of pex34 Δ pex25 Δ cells upon inducing and non-inducing conditions.…”
Section: Resultsmentioning
confidence: 99%
“…As Pex25p has also been implicated in de novo synthesis of peroxisomes in H. polymorpha (Saraya et al, 2011) and S. cerevisiae (Huber et al, 2012), and as Pex25p and Pex34p do interact, we investigated whether both proteins function in concert in the de novo formation of peroxisomes and studied this process in the pex34 Δ pex25 Δ double mutant. Cells concurrently lacking Pex25p and Pex34p are characterized by a severe import defect for the otherwise peroxisomal Mdh2-GFP (Tower et al, 2011) and GFP-SKL under inducing conditions ( FIG 6 ).…”
Section: Discussionmentioning
confidence: 99%
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“…Plasmids pRDV1 and pRDV2 were constructed as follows: plasmids pZ15-MycUb and pZ15-MycUb K48R, which contain wild type or K48R forms of Myc tagged ubiquitin, under control of the dihydroxyacetone synthase (P DHAS ) promoter [23] were digested with NotI and Bpu10I and the resulting fragments were ligated into NotI-Bpu10I digested pHIPH4 [24], creating pRDV1 (P DHAS Myc-Ub) and pRDV2 (P DHAS Myc-Ub K48R). Plasmids pRDV1 and pRDV2 were linearised with BstBI in the P DHAS region and integrated into the H. polymorpha genome.…”
Section: Cloning and Plasmidsmentioning
confidence: 99%