The twin-arginine translocation (Tat) pathway in Corynebacterium glutamicum has been described previously. The minimal functional Tat system in C. glutamicum required TatA and TatC but did not require TatB, although this component was required for maximal efficiency of Tat-dependent secretion. We previously demonstrated that Chryseobacterium proteolyticum pro-protein glutaminase (pro-PG) and Streptomyces mobaraensis pro-transglutaminase (pro-TG) could be secreted via the Tat pathway in C. glutamicum. Here we report that the amounts of pro-PG secreted were more than threefold larger when TatC or TatAC was overexpressed, and there was a further threefold increase when TatABC was overexpressed. These results show that the amount of TatC protein is the first bottleneck and the amount of TatB protein is the second bottleneck in Tat-dependent protein secretion in C. glutamicum. In addition, the amount of pro-TG that accumulated via the Tat pathway when TatABC was overexpressed with the TorA signal peptide in C. glutamicum was larger than the amount that accumulated via the Sec pathway. We concluded that TatABC overexpression improves Tat-dependent pro-PG and pro-TG secretion in C. glutamicum.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2632119PMC
http://dx.doi.org/10.1128/AEM.01874-08DOI Listing

Publication Analysis

Top Keywords

tat pathway
12
tatabc overexpression
8
overexpression improves
8
corynebacterium glutamicum
8
tat-dependent protein
8
protein secretion
8
tatabc overexpressed
8
secretion glutamicum
8
glutamicum
7
tatabc
4

Similar Publications

Electrocatalytic CO2 reduction (CO2R) to multi-carbon (C2+) products in strong acid presents a promising approach to mitigate the CO2 loss commonly encountered in alkaline and neutral systems. However, this process often suffers from low selectivity for C2+ products due to the competing C1 (e.g.

View Article and Find Full Text PDF

PF1163A () is a fungal metabolite that inhibits sterol-C4-methyl oxidase. In this study, we identified the biosynthetic gene cluster of and elucidated its biosynthetic pathway through heterologous expression experiments. Polyketide synthase-nonribosomal synthetase hybrid PfaA, which is responsible for the biosynthesis of PF1163A, harbors an unusual domain organization with tandem condensation (C) domains and a terminal condensation domain.

View Article and Find Full Text PDF

SENP6-Mediated deSUMOylation of Nrf2 Exacerbates Neuronal Oxidative Stress Following Cerebral Ischemia and Reperfusion Injury.

Adv Sci (Weinh)

December 2024

Department of Anesthesiology and Pain Medicine, Hubei Key Laboratory of Geriatric Anesthesia and Perioperative Brain Health, and Wuhan Clinical Research Center for Geriatric Anesthesia, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.

Oxidative stress is believed to play critical pathophysiological roles in ischemic brain injury, and the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway is recognized as the most crucial endogenous antioxidant stress damage route. Some research have demonstrated that Nrf2 play critical roles in oxidative stress after ischemic stroke, but the underlying mechanism are not fully elucidated. This study reveals that Nrf2 is modified by SUMOylation and identifies Sentrin/SUMO-specific protease 6 (SENP6) as a negative regulator of Nrf2 SUMOylation.

View Article and Find Full Text PDF

Methamphetamine and HIV-1 Tat Protein Synergistically Induce Endoplasmic Reticulum Stress to Promote TRIM13-Mediated Neuronal Autophagy.

Mol Neurobiol

December 2024

NHC Key Laboratory of Drug Addiction Medicine, School of Forensic Medicine, Kunming Medical University, 1168 West Chunrong Road, Yuhua Avenue Chenggong District, Kunming, 650500, China.

Co-exposure to methamphetamine (METH) abuse and HIV infection exacerbates central nervous system damage. However, the underlying mechanisms of this process remain poorly understood. This study aims to explore the roles of neuronal autophagy in the synergistic damage to the central nervous system caused by METH and HIV proteins.

View Article and Find Full Text PDF

Targeting nonapoptotic cell death offers a promising strategy for overcoming apoptosis resistance in cancer. In this study, we developed Tat-Ram13, a 25-mer peptide that fuses the NOTCH1 intracellular domain fragment RAM13 with a cell-penetrating HIV-1 TAT, for the treatment of T-cell acute lymphoblastic leukemia with aberrant NOTCH1 mutation. Tat-Ram13 significantly downregulated NOTCH1-target genes in T-ALL cell lines.

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!