Ras-MAPK pathway participates of the nitrosative stress response in pathogenic fungus Paracoccidioides brasiliensis
Paracoccidioides
Pathogenic fungus
DOI:
10.26226/morressier.5ac39996d462b8028d89a050
Publication Date:
2020-02-19T17:12:24Z
AUTHORS (2)
ABSTRACT
Ras-MAPK pathway participates of the nitrosative stress response in pathogenic fungus Paracoccidioides brasiliensisParacoccidioides brasiliensis is a temperature-dependent dimorphic that cause paracoccidioidomycosis (PCM).The capacity to evade innate immune host due its ability respond and survive caused by cells system.However, regulation signal transduction pathways associated are poorly understood.Ras GTPases (Ras1 Ras2) well known regulate antagonistically or cooperatively various cellular events many fungi.Ras, activated form (Ras-GTP), interacts with effector proteins can initiate kinase cascade.In lower eukaryotes, Byr2 represents Ras target.In present study, we investigated role GTPase P. after vitro stimulus nitric oxide (NO).We observed low concentrations NO induce cell proliferation brasiliensis, while high promoted decrease fungal viability.Additionally, observe both (cell death) reversed presence scavenger (carboxy-PTIO).We reported immunobloting stimulation NO, active was extracts.High induces S-nitrosylation and, this conditions, modulates expression antioxidant genes stress.We also whether Hog-1 would be stress.Under these conditions phosphorylated treatment.In addition, when used RBD-GST probe blotted anti-Hog-1 antibody Ras-GTP interact MAPK NO.Finally, our data indicate may cross-talk brasiliensis.S-nitrosylation probably activates GTPase, which initiates signaling cascade involving Ras-Byr2-By1-Hog.These responses could help their initial contacts system, crucial for disease establishment.
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