Vti1a/b support distinct aspects of TGN and cis-/medial Golgi organization.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
02 12 2022
Historique:
received: 15 07 2022
accepted: 28 11 2022
entrez: 2 12 2022
pubmed: 3 12 2022
medline: 7 12 2022
Statut: epublish

Résumé

Retrograde trafficking towards the trans-Golgi network (TGN) is important for dense core vesicle (DCV) biogenesis. Here, we used Vti1a/b deficient neurons to study the impact of disturbed retrograde trafficking on Golgi organization and cargo sorting. In Vti1a/b deficient neurons, staining intensity of cis-/medial Golgi proteins (e.g., GM130 and giantin) was increased, while the intensity of two recycling TGN proteins, TGN38 and TMEM87A, was decreased and the TGN-resident protein Golgin97 was normal. Levels and localization of DCV cargo markers, LAMP1 and KDEL were also altered. This phenotype was not caused by reduced Golgi size or absence of a TGN compartment. The phenotype was partially phenocopied by disturbing sphingolipid homeostasis, but was not rescued by overexpression of sphingomyelin synthases or the sphingolipid synthesis inhibitor myriocin. We conclude that Vti1a/b are important for distinct aspects of TGN and cis-/medial Golgi organization. Our data underline the importance of retrograde trafficking for Golgi organization, DCV cargo sorting and the distribution of proteins of the regulated secretory pathway.

Identifiants

pubmed: 36460703
doi: 10.1038/s41598-022-25331-x
pii: 10.1038/s41598-022-25331-x
pmc: PMC9718741
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

20870

Informations de copyright

© 2022. The Author(s).

Références

Mol Biol Cell. 2017 Dec 15;28(26):3870-3880
pubmed: 29074564
Traffic. 2006 Feb;7(2):191-204
pubmed: 16420527
FEBS Lett. 2019 Sep;593(17):2466-2487
pubmed: 31381138
Elife. 2015 Sep 10;4:
pubmed: 26357016
EMBO J. 2004 Jan 14;23(1):33-44
pubmed: 14685263
Elife. 2016 Oct 18;5:
pubmed: 27751232
Cell. 1991 Nov 1;67(3):601-16
pubmed: 1682055
Proc Natl Acad Sci U S A. 2011 Feb 8;108(6):2575-80
pubmed: 21262811
J Cell Biol. 2012 Dec 10;199(6):883-91
pubmed: 23229896
Front Mol Neurosci. 2018 Jan 23;11:10
pubmed: 29410613
Trends Cell Biol. 2010 Jun;20(6):329-36
pubmed: 20227882
Ann N Y Acad Sci. 2019 Nov;1455(1):59-80
pubmed: 31271235
Mol Psychiatry. 2013 Jun;18(6):646-55
pubmed: 22801411
Chem Phys Lipids. 2018 Nov;216:114-131
pubmed: 30194926
Mol Biol Cell. 2008 Jun;19(6):2350-62
pubmed: 18367545
Science. 1996 May 24;272(5265):1161-3
pubmed: 8638159
J Cell Biol. 2020 Mar 2;219(3):
pubmed: 32045479
Exp Cell Res. 2021 Feb 15;399(2):112442
pubmed: 33359467
J Cell Sci. 1995 Jun;108 ( Pt 6):2405-14
pubmed: 7545686
J Cell Sci. 2017 Jun 1;130(11):1877-1889
pubmed: 28404788
J Neurosci. 2009 Jan 7;29(1):23-37
pubmed: 19129381
Proc Natl Acad Sci U S A. 2020 May 12;117(19):10565-10574
pubmed: 32345721
Mol Syst Biol. 2012;8:629
pubmed: 23212246
Nutr Metab (Lond). 2012 Jul 31;9(1):71
pubmed: 22849442
Physiology (Bethesda). 2006 Apr;21:124-33
pubmed: 16565478
Biochim Biophys Acta. 1976 Dec 2;455(2):433-51
pubmed: 999922
Nat Methods. 2012 Jun 28;9(7):676-82
pubmed: 22743772
Prog Neurobiol. 2005 Jun;76(2):99-125
pubmed: 16099088
J Cell Sci. 2001 Dec;114(Pt 24):4543-55
pubmed: 11792819
Mol Biol Cell. 1993 Jan;4(1):93-105
pubmed: 8443412
PLoS One. 2011;6(9):e23644
pubmed: 21980337
J Neurosci. 2017 Apr 26;37(17):4525-4539
pubmed: 28348137
Nutr Metab (Lond). 2011 Dec 14;8:89
pubmed: 22168400
Proc Natl Acad Sci U S A. 2008 Mar 4;105(9):3351-6
pubmed: 18308930
Front Neurosci. 2015 Oct 21;9:381
pubmed: 26539077
J Biol Chem. 2010 Dec 31;285(53):41472-82
pubmed: 21047787
Brain Res Mol Brain Res. 2004 Aug 23;127(1-2):68-78
pubmed: 15306122
J Biol Chem. 2002 May 3;277(18):16011-21
pubmed: 11854265
Mol Biol Cell. 2005 Mar;16(3):1555-67
pubmed: 15647381
Neuropeptides. 2010 Jun;44(3):215-24
pubmed: 20096456
Mol Biol Cell. 2015 Sep 1;26(17):3071-84
pubmed: 26157166
J Cell Sci. 2000 Sep;113 ( Pt 18):3299-307
pubmed: 10954427
Nat Commun. 2018 Aug 24;9(1):3421
pubmed: 30143604

Auteurs

Danique M van Bommel (DM)

Department of Functional Genomics, Center for Neurogenomics and Cognitive Research (CNCR), Vrije Universiteit (VU) Amsterdam, De Boelelaan 1085, Amsterdam, 1081 HV, The Netherlands.

Ruud F Toonen (RF)

Department of Functional Genomics, Center for Neurogenomics and Cognitive Research (CNCR), Vrije Universiteit (VU) Amsterdam, De Boelelaan 1085, Amsterdam, 1081 HV, The Netherlands.

Matthijs Verhage (M)

Department of Functional Genomics, Center for Neurogenomics and Cognitive Research (CNCR), Vrije Universiteit (VU) Amsterdam, De Boelelaan 1085, Amsterdam, 1081 HV, The Netherlands. matthijs@cncr.vu.nl.
Functional Genomics, Department of Human Genetics, Center for Neurogenomics and Cognitive Research (CNCR), UMC Amsterdam, De Boelelaan 1085, Amsterdam, 1081 HV, The Netherlands. matthijs@cncr.vu.nl.

Articles similaires

Pathogenic mitochondrial DNA mutations inhibit melanoma metastasis.

Spencer D Shelton, Sara House, Luiza Martins Nascentes Melo et al.
1.00
DNA, Mitochondrial Humans Melanoma Mutation Neoplasm Metastasis

Kupffer cell reverse migration into the liver sinusoids mitigates neonatal sepsis and meningitis.

Bruna Araujo David, Jawairia Atif, Fernanda Vargas E Silva Castanheira et al.
1.00
Animals Kupffer Cells Mice Liver Cell Movement

A key role for P2RX5 in brown adipocyte differentiation and energy homeostasis.

Maria Razzoli, Seth McGonigle, Bhavani Shankar Sahu et al.
1.00
Animals Adipocytes, Brown Mice Cell Differentiation Male
Female Humans Gonadotropin-Releasing Hormone Stromal Cells Embryo Implantation

Classifications MeSH