The Endoplasmic Reticulum-Plasma Membrane Tethering Protein Ice2 Controls Lipid Droplet Size via the Regulation of Phosphatidylcholine in .

Lipid droplets (LDs) are intracellular organelles that play important roles in cellular lipid metabolism; they change their sizes and numbers in response to both intracellular and extracellular signals. Changes in LD size reflect lipid synthesis and degradation and affect many cellular activities, including energy supply and membrane synthesis. Here, we focused on the function of the endoplasmic reticulum-plasma membrane tethering protein Ice2 in LD dynamics in the fungal pathogen ().

Mec1-Rad53 Signaling Regulates DNA Damage-Induced Autophagy and Pathogenicity in .

DNA damage activates the DNA damage response and autophagy in ; however, the relationship between the DNA damage response and DNA damage-induced autophagy in remains unclear. Mec1-Rad53 signaling is a critical pathway in the DNA damage response, but its role in DNA damage-induced autophagy and pathogenicity in remains to be further explored. In this study, we compared the function of autophagy-related (Atg) proteins in DNA damage-induced autophagy and traditional macroautophagy and explored the role of Mec1-Rad53 signaling in regulating DNA damage-induced autophagy and pathogenicity.

Reduction of histone proteins dosages increases CFW sensitivity and attenuates virulence of Candida albicans.

Histone proteins are important components of nucleosomes, which play an important role in regulating the accessibility of DNA and the function of genomes. However, the effect of histone proteins dosages on physiological processes is not clear in the human fungal pathogen Candida albicans. In this study, we found that the deletion of the histone protein H3 coding gene HHT21 and the histone protein H4 coding gene HHF1 resulted in a significant decrease in the expression dosage of the histone proteins H3 and H4, which had a significant impact on the localization of the histone protein H2A and plasmid maintenance.

DNA damage-induced autophagy is regulated by inositol polyphosphate synthetases in Candida albicans.

DNA damage-induced autophagy is a new type of autophagy that differs from traditional macroautophagy; however, this type of autophagy has not been identified in the pathogenic fungus Candida albicans. Inositol polyphosphates are involved in the regulation of DNA damage repair and macroautophagy; however, whether inositol polyphosphates are involved in the regulation of DNA damage-induced autophagy remains unclear. In this study, we identified DNA damage-induced autophagy in C.

Gallium-based metal-organic frameworks loaded with antimicrobial peptides for synergistic killing of drug-resistant bacteria.

Increased antibiotic resistance has made bacterial infections a global concern, which requires novel non-antibiotic-dependent antibacterial strategies to address the menace. Antimicrobial peptides (AMPs) are a promising antibiotic alternative, whose antibacterial mechanism is mainly to destroy the membrane of bacteria. Gallium ions exhibit an antibacterial effect by interfering with the iron metabolism of bacteria.

The Tricalbin-Family Endoplasmic Reticulum-Plasma Membrane Tethering Proteins Attenuate ROS-Involved Caspofungin Sensitivity in Candida albicans.

The endoplasmic reticulum-plasma membrane (ER-PM) contacts are one kind of important membrane contact structures in eukaryotic cells, which mediate material and message exchange between the ER and the PM. However, the specific types and functions of ER-PM tethering proteins are poorly understood in the human fungal pathogen Candida albicans. In this study, we observed that the two tricalbin-family proteins, i.

Pathogen infection-responsive nanoplatform targeting macrophage endoplasmic reticulum for treating life-threatening systemic infection.

Unlabelled: Systemic infections caused by life-threatening pathogens represent one of the main factors leading to clinical death. In this study, we developed a pathogen infection-responsive and macrophage endoplasmic reticulum-targeting nanoplatform to alleviate systemic infections. The nanoplatform is composed of large-pore mesoporous silica nanoparticles (MSNs) grafted by an endoplasmic reticulum-targeting peptide, and a pathogen infection-responsive cap containing the reactive oxygen species-cleavable boronobenzyl acid linker and bovine serum albumin.

The V-ATPase regulates localization of the TRP Ca channel Yvc1 in response to oxidative stress in Candida albicans.

The vacuolar-type H-ATPase (V-ATPase) is a highly conserved protein complex among the eukaryotic cells. We previously revealed that both the V-ATPase and the transient receptor potential (TRP) channel Yvc1 are involved in oxidative stress response (OSR). However, the relationship between V-ATPase and Yvc1 during OSR remains unknown.

The inositol polyphosphate kinase Ipk1 transcriptionally regulates mitochondrial functions in Candida albicans.

Inositol polyphosphates (IPs) is an important family of signaling molecules that regulate multiple cellular processes, such as chromatin remodeling, transcription and mRNA export. Inositol polyphosphate kinases, as the critical enzymes for production and transformation of IPs, directly determine the intracellular levels of IPs and therefore are involved in many cellular processes. However, its roles in Candida albicans, the leading fungal pathogen in human beings, remain to be investigated.

Candida albicans infection disturbs the redox homeostasis system and induces reactive oxygen species accumulation for epithelial cell death.

Candida albicans is a common pathogenic fungus with high mortality in immunocompromised patients. However, the mechanism by which C. albicans invades host epithelial cells and causes serious tissue damage remains to be further investigated.