29 research outputs found
The Aspergillus nidulans syntaxin PepA(Pep12) is regulated by two Sec1/Munc-18 proteins to mediate fusion events at early endosomes, late endosomes and vacuoles.
The toxic mechanism and bioactive components of Chinese leek root exudates acting against Fusarium oxysporum f. sp. cubense tropical race 4
Genetic studies on the physiological role of CORVET in Aspergillus nidulans.
CORVET and HOPS are protein complexes mediating the maturation of early endosomes (EEs) into late endosomes (LEs)/vacuoles. These hetero-hexamers share four 'core' components, Vps11, Vps16, Vps18 and Vps33, and differ in two specific subunits, CORVET Vps8 and Vps3 and HOPS Vps39 and Vps41. Whereas ablating HOPS-specific components has minor growth effects, ablating any CORVET constituent severely debilitates Aspergillus nidulans growth, buttressing previous work indicating that maturation of EEs into LEs is physiologically crucial. A genetic screen revealed that impairing the slt cation homeostasis pathway rescues the growth defect resulting from inactivation of the 'core' protein Vps33. Subsequent genetic analyses showed that the defect resulting from lack of any one of the five other CORVET components could similarly be rescued by sltAÎ eliminating the slt regulator SltA. Whereas double deletants lacking functionally non-equivalent components of the CORVET and HOPS complexes are rescued by sltAÎ, those lacking functionally equivalent components are not, suggesting that intermediate 'hybrid' complexes previously detected in yeast are physiologically relevant. vps3Î, vps8Î, vps39Î and vps41Î result in small vacuoles. This phenotype is remediable by sltAÎ in the case of CORVET-specific, but not in the case of HOPS-specific deletants, indicating that the slt- effect on vacuolar size necessitates HOPS
Fungal pathogen uses sex pheromone receptor for chemotropic sensing of host plant signals
Nitrogen deprivation in Fusarium oxysporum promotes mycotoxin production via intermediates in the Krebs cycle and unreported methylmalonyl-CoA mutase activity
No to Neocosmospora: Phylogenomic and Practical Reasons for Continued Inclusion of the Fusarium solani Species Complex in the Genus Fusarium.
This article is to alert medical mycologists and infectious disease specialists of recent name changes of medically important species of the filamentous mold Fusarium Fusarium species can cause localized and life-threating infections in humans. Of the 70 Fusarium species that have been reported to cause infections, close to one-third are members of the Fusarium solani species complex (FSSC), and they collectively account for approximately two-thirds of all reported Fusarium infections. Many of these species were recently given scientific names for the first time by a research group in the Netherlands, but they were misplaced in the genus Neocosmospora In this paper, we present genetic arguments that strongly support inclusion of the FSSC in Fusarium There are potentially serious consequences associated with using the name Neocosmospora for Fusarium species because clinicians need to be aware that fusaria are broadly resistant to the spectrum of antifungals that are currently available