The putative prenyltransferase Nus1 is required for filamentation in the human fungal pathogen Candida albicans.

Candida albicans is a major fungal pathogen of humans that can cause serious systemic infections in vulnerable immunocompromised populations. One of its virulence attributes is its capacity to transition between yeast and filamentous morphologies, but our understanding of this process remains incomplete. Here, we analyzed data from a functional genomic screen performed with the C.

Respiration supports intraphagosomal filamentation and escape of from macrophages.

is a leading human fungal pathogen that often causes life-threatening infections in immunocompromised individuals. The ability of to transition between yeast and filamentous forms is key to its virulence, and this occurs in response to many host-relevant cues, including engulfment by host macrophages. While previous efforts identified genes required for filamentation in other conditions, the genes important for this morphological transition upon internalization by macrophages remained largely enigmatic.

DYRK-family kinases regulate morphogenesis and virulence through the Ras1/PKA pathway.

is an opportunistic human fungal pathogen that frequently causes life-threatening infections in immunocompromised individuals. To cause disease, the fungus employs several virulence traits, including its ability to transition between yeast and filamentous states. Previous work identified a role for the kinase Yak1 in regulating filamentation.

Construction of Candida albicans Strains with ATP-Analog-Sensitive Protein Kinase A and Hog1.

Candida albicans is an opportunistic human fungal pathogen and a member of the mucosal microbiota. To survive in the host and cause disease, C. albicans utilizes several virulence traits, including the ability to respond and adapt to diverse stressors, as well as the morphogenetic switch between yeast and filamentous morphologies.

Functional genomic analysis of protein kinases reveals modulators of morphogenesis in diverse environments.

is a leading cause of mycotic infection. The ability to transition between yeast and filamentous forms is critical to virulence and complex signaling pathways regulate this process. Here, we screened a protein kinase mutant library in six environmental conditions to identify regulators of morphogenesis.

Bacterial-fungal interactions and their impact on microbial pathogenesis.

Microbial communities of the human microbiota exhibit diverse effects on human health and disease. Microbial homeostasis is important for normal physiological functions and changes to the microbiota are associated with many human diseases including diabetes, cancer, and colitis. In addition, there are many microorganisms that are either commensal or acquired from environmental reservoirs that can cause diverse pathologies.

A small molecule produced by Lactobacillus species blocks Candida albicans filamentation by inhibiting a DYRK1-family kinase.

The fungus Candida albicans is an opportunistic pathogen that can exploit imbalances in microbiome composition to invade its human host, causing pathologies ranging from vaginal candidiasis to fungal sepsis. Bacteria of the genus Lactobacillus are colonizers of human mucosa and can produce compounds with bioactivity against C. albicans.

High-Throughput Screening Identifies Genes Required for Induction of Macrophage Pyroptosis.

The innate immune system is the first line of defense against invasive fungal infections. As a consequence, many successful fungal pathogens have evolved elegant strategies to interact with host immune cells. For example, undergoes a morphogenetic switch coupled to cell wall remodeling upon phagocytosis by macrophages and then induces macrophage pyroptosis, an inflammatory cell death program.

The effects of CO(2) and chronic cold exposure on fecundity of female Drosophila melanogaster.

Carbon dioxide and chilling are sometimes used to immobilise insects for laboratory research. Both of these methods are known to have short-term effects on behaviour and physiology in Drosophila, but their long-term impacts are unknown. We exposed female D.