Distinct adaptor proteins assist exit of Kre2-family proteins from the yeast ER.

Biol Open

Department of Biotechnology, University of Tokyo, Yayoi, Bunkyo-Ku, Tokyo 113-8657, Japan.

Published: March 2014

The Svp26 protein of S. cerevisiae is an ER- and Golgi-localized integral membrane protein with 4 potential membrane-spanning domains. It functions as an adaptor protein that facilitates the ER exit of Ktr3, a mannosyltransferase required for biosynthesis of O-linked oligosaccharides, and the ER exit of Mnn2 and Mnn5, mannosyltransferases, which participate in the biosynthesis of N-linked oligosaccharides. Ktr3 belongs to the Kre2 family, which consists of 9 members of type-II membrane proteins sharing sequence similarities. In this report, we examined all Kre2 family members and found that the Golgi localizations of two others, Kre2 and Ktr1, were dependent on Svp26 by immunofluorescence microscopy and cell fractionations in sucrose density gradients. We show that Svp26 functions in facilitating the ER exit of Kre2 and Ktr1 by an in vitro COPII budding assay. Golgi localization of Ktr4 was not dependent on Svp26. Screening null mutants of the genes encoding abundant COPII membrane proteins for those showing mislocalization of Ktr4 in the ER revealed that Erv41 and Erv46 are required for the correct Golgi localization of Ktr4. We provide biochemical evidence that the Erv41-Erv46 complex functions as an adaptor protein for ER exit of Ktr4. This is the first demonstration of the molecular function of this evolutionally conserved protein complex. The domain switching experiments show that the lumenal domain of Ktr4 is responsible for recognition by the Erv41-Erv46 complex. Thus, ER exit of Kre2-family proteins is dependent on distinct adaptor proteins and our results provide new insights into the traffic of Kre2-family mannosyltransferases.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4001239PMC
http://dx.doi.org/10.1242/bio.20146312DOI Listing

Publication Analysis

Top Keywords

distinct adaptor
8
adaptor proteins
8
exit kre2-family
8
kre2-family proteins
8
functions adaptor
8
adaptor protein
8
kre2 family
8
membrane proteins
8
kre2 ktr1
8
dependent svp26
8

Similar Publications

Article Synopsis
  • Researchers have identified genetic polymorphisms of ABI3 as a risk factor for late-onset Alzheimer's Disease (LOAD), but the role of ABI3 in microglia is not well understood.
  • Using CRISPR/Cas9, a specific risk variant (S212F) was introduced into mouse models to study its effects on AD-related pathologies alongside 5xFAD mice over time.
  • Results showed that the 5xFAD/Abi3 mice exhibited a decrease in amyloid beta plaque burden and a significant reduction in microglia numbers with age, suggesting ABI3 may influence both plaque formation and microglial response in AD pathology.
View Article and Find Full Text PDF

ECSIT-X4 is Required for Preventing Pressure Overload-Induced Cardiac Hypertrophy via Regulating Mitochondrial STAT3.

Adv Sci (Weinh)

January 2025

Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, School of Basic Medical Sciences, Nanjing Medical University, Nanjing, Jiangsu, 211166, China.

Mitochondrial dysfunction is a key factor in exacerbating pressure overload-induced cardiac hypertrophy and is linked to increased morbidity and mortality. ECSIT, a crucial adaptor for inflammation and mitochondrial function, has been reported to express multiple transcripts in various species and tissues, leading to distinct protein isoforms with diverse subcellular localizations and functions. However, whether an unknown ECSIT isoform exists in cardiac cells and its potential role in regulating mitochondrial function and pathological cardiac hypertrophy has remained unclear.

View Article and Find Full Text PDF

The microtubule motor cytoplasmic dynein-1 transports and positions various organelles, but the molecular basis of this functional diversity is not fully understood. Cargo adaptors of the Hook protein family recruit dynein to early endosomes (EE) in fungi and human cells by forming the FTS-Hook-FHIP (FHF) complex. By contrast, the Hook homolog ZYG-12 recruits dynein to the nuclear envelope (NE) in the meiotic gonad and mitotic early embryo by forming a Linker of Nucleoskeleton and Cytoskeleton (LINC) complex.

View Article and Find Full Text PDF

LASP1 inhibits the formation of NETs and alleviates acute pancreatitis by stabilizing F-actin polymerization in neutrophils.

Biochem Biophys Res Commun

January 2025

Department of Gastroenterology, Kunshan Hospital of Traditional Chinese Medicine, Yangzhou University, Kunshan, Suzhou, Jiangsu, China. Electronic address:

Background: Neutrophil extracellular traps (NETs) play a significant role in the development of acute pancreatitis (AP). The actin-binding protein LASP1 regulates proteins associated with the cytoskeleton, yet its precise involvement in NETs and AP remains to be elucidated.

Methods: To investigate the role of LASP1 in NETs and AP, several bioinformatics methods, such as weighted gene co-expression network analysis (WGCNA), differential analysis, and least absolute shrinkage and selection operator (LASSO) regression, were utilized to screen for feature genes based on the Gene Expression Omnibus (GEO) dataset.

View Article and Find Full Text PDF

Immune responses to tumors, comprising adaptive T cells and innate NK cells, arise very early in tumorigeneses and prior to detection of palpable tumors or before tissue pathology is evident. Yet, how nascent tumors evoke dendritic cell maturation and the resulting cytokine responses that are necessary for these effector anti-tumor immune responses is unknown. We have previously shown that CD91 expression on dendritic cells is important for immune surveillance, specifically for generating T cell and NK cell responses to nascent tumors.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!