We have carried out an in silico exploration of the genomes of Aspergillus nidulans, Aspergillus fumigatus, and Aspergillus oryzae, and identified components of G-protein/cAMP-mediated signaling. Putative G-protein coupled receptors (GPCRs) were distributed over nine classes. The GPCRs within classes were well conserved among aspergilli but varied in other ascomycetes. As previously observed in A. nidulans and other fungi, three Galpha, one Gbeta, and one Ggamma subunits of G proteins were identified in A. fumigatus, whereas an additional likely non-functional Galpha subunit was present in A. oryzae. While most fungal species had five proteins containing the regulator of G-protein signaling (RGS) domain predicted to participate in attenuation of G-protein signaling, A. fumigatus and A. oryzae had an additional RGS protein (RgsD) related to RgsA of A. nidulans. Genes encoding adenylate cyclase, a regulatory subunit and two catalytic subunits of the cAMP-dependent protein kinase, were also identified in the three aspergilli. Finally, regulators of cAMP signaling including low- and high-affinity phosphodiesterases were identified. Taken together, our data indicate a striking diversity at the GPCR level, but little diversity of components at the G-protein and cAMP-signaling level. This may reflect the abilities of these fungi to adapt to various ecological niches and to integrate diverse environmental cues into highly conserved cellular processes.
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http://dx.doi.org/10.1016/j.fgb.2006.02.001 | DOI Listing |
Liver Int
February 2025
Division of Bioinformatics and Statistics, The FDA's National Center for Toxicological Research, Jefferson, Arkansas, USA.
Background And Aims: Acute liver failure (ALF) is a serious condition, typically in individuals without prior liver disease. Drug-induced ALF (DIALF) constitutes a major portion of ALF cases. Our research aimed to identify potential genetic predispositions to DIALF.
View Article and Find Full Text PDFJ Cell Biol
April 2025
Department of Genetics and Cell Biology, College of Life Sciences, State Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin, China.
TBC1D20 deficiency causes Warburg Micro Syndrome in humans, characterized by multiple eye abnormalities, severe intellectual disability, and abnormal sexual development, but the molecular mechanisms remain unknown. Here, we identify TBC1D20 as a novel Rab11 GTPase-activating protein that coordinates vesicle transport and actin remodeling to regulate ciliogenesis. Depletion of TBC1D20 promotes Rab11 vesicle accumulation and actin deconstruction around the centrosome, facilitating the initiation of ciliogenesis even in cycling cells.
View Article and Find Full Text PDFUnlabelled: SYNGAP1 is a key Ras-GAP protein enriched at excitatory synapses, with mutations causing intellectual disability and epilepsy in humans. Recent studies have revealed that in addition to its role as a negative regulator of G-protein signaling through its GAP enzymatic activity, SYNGAP1 plays an important structural role through its interaction with post-synaptic density proteins. Here, we reveal that intrinsic excitability deficits and seizure phenotypes in heterozygous Syngap1 knockout (KO) mice are differentially dependent on Syngap1 GAP activity.
View Article and Find Full Text PDFUnlabelled: 20-carbon fatty acid-derived eicosanoids are versatile signaling oxylipins in mammals. In particular, a group of eicosanoids termed prostanoids are involved in multiple physiological processes, such as reproduction and immune responses. Although some eicosanoids such as prostaglandin E2 (PGE2) have been detected in some insect species, molecular mechanisms of eicosanoid synthesis and signal transduction in insects have been poorly investigated.
View Article and Find Full Text PDFCancer Manag Res
January 2025
Department of Thoracic Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Background: Signaling pathways centered on the G-protein ADP-ribosylation factor 6 (Arf6) and its downstream effector ArfGAP with the SH3 Domain, Ankyrin Repeat and PH Domain 1 (AMAP1) drive cancer invasion, metastasis, and therapy resistance. The Arf6-AMAP1 pathway has been reported to promote receptor recycling leading to programmed cell death-ligand 1 (PD-L1) overexpression in pancreatic ductal carcinoma. Moreover, AMAP1 regulates of nuclear factor-kappa B (NF-κB), which is an important molecule in inflammation and immune activation, including tumor immune interaction through PD-L1 regulation.
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