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Aspergillus oxylipin signaling and quorum sensing pathways depend on g protein-coupled receptors.

Affeldt KJ, Brodhagen M, Keller NP - Toxins (Basel) (2012)

Bottom Line: Here, we present evidence that oxylipins stimulate a burst in cAMP in A. nidulans, and that loss of an A. nidulans GPCR, gprD, prevents this cAMP accumulation.A. flavus undergoes an oxylipin-mediated developmental shift when grown at different densities, and this regulates spore, sclerotial and aflatoxin production.The finding of GPCRs that regulate production of survival structures (sclerotia), inoculum (spores) and aflatoxin holds promise for future development of anti-fungal therapeutics.

View Article: PubMed Central - PubMed

Affiliation: Department of Bacteriology and Department of Medical Microbiology and Immunology, 1550 Linden Drive, Madison, WI 53706, USA.

ABSTRACT
Oxylipins regulate Aspergillus development and mycotoxin production and are also involved in Aspergillus quorum sensing mechanisms. Despite extensive knowledge of how these oxylipins are synthesized and what processes they regulate, nothing is known about how these signals are detected and transmitted by the fungus. G protein-coupled receptors (GPCR) have been speculated to be involved as they are known oxylipin receptors in mammals, and many putative GPCRs have been identified in the Aspergilli. Here, we present evidence that oxylipins stimulate a burst in cAMP in A. nidulans, and that loss of an A. nidulans GPCR, gprD, prevents this cAMP accumulation. A. flavus undergoes an oxylipin-mediated developmental shift when grown at different densities, and this regulates spore, sclerotial and aflatoxin production. A. flavus encodes two putative GprD homologs, GprC and GprD, and we demonstrate here that they are required to transition to a high-density development state, as well as to respond to spent medium of a high-density culture. The finding of GPCRs that regulate production of survival structures (sclerotia), inoculum (spores) and aflatoxin holds promise for future development of anti-fungal therapeutics.

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Samples were treated with EtOH (control) or 10 μM 13(S)-HpODE in EtOH. Tissues were harvested as described, and cAMP concentrations were measured. Differences from the EtOH control are denoted as follows: *p < 0.05, determined by a one-tailed paired Student’s T-test.
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toxins-04-00695-f007: Samples were treated with EtOH (control) or 10 μM 13(S)-HpODE in EtOH. Tissues were harvested as described, and cAMP concentrations were measured. Differences from the EtOH control are denoted as follows: *p < 0.05, determined by a one-tailed paired Student’s T-test.

Mentions: As a final control to confirm accuracy of our methodology, we assessed an adenylate cyclase mutant (∆cyaA, [44]) and its parental wild type cyaA strain for their responses to 13(S)-HpODE. Adenylate cyclase is required for activation of cAMP release. As expected, addition of 13(S)-HpODE to the wild type increased cAMP production 1.8 fold over the EtOH control (p = 0.05). However, there was no significant difference between samples of the ∆cyaA mutant treated with EtOH or 13(S)-HpODE (p = 1.4; Figure S1).


Aspergillus oxylipin signaling and quorum sensing pathways depend on g protein-coupled receptors.

Affeldt KJ, Brodhagen M, Keller NP - Toxins (Basel) (2012)

Samples were treated with EtOH (control) or 10 μM 13(S)-HpODE in EtOH. Tissues were harvested as described, and cAMP concentrations were measured. Differences from the EtOH control are denoted as follows: *p < 0.05, determined by a one-tailed paired Student’s T-test.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3475224&req=5

toxins-04-00695-f007: Samples were treated with EtOH (control) or 10 μM 13(S)-HpODE in EtOH. Tissues were harvested as described, and cAMP concentrations were measured. Differences from the EtOH control are denoted as follows: *p < 0.05, determined by a one-tailed paired Student’s T-test.
Mentions: As a final control to confirm accuracy of our methodology, we assessed an adenylate cyclase mutant (∆cyaA, [44]) and its parental wild type cyaA strain for their responses to 13(S)-HpODE. Adenylate cyclase is required for activation of cAMP release. As expected, addition of 13(S)-HpODE to the wild type increased cAMP production 1.8 fold over the EtOH control (p = 0.05). However, there was no significant difference between samples of the ∆cyaA mutant treated with EtOH or 13(S)-HpODE (p = 1.4; Figure S1).

Bottom Line: Here, we present evidence that oxylipins stimulate a burst in cAMP in A. nidulans, and that loss of an A. nidulans GPCR, gprD, prevents this cAMP accumulation.A. flavus undergoes an oxylipin-mediated developmental shift when grown at different densities, and this regulates spore, sclerotial and aflatoxin production.The finding of GPCRs that regulate production of survival structures (sclerotia), inoculum (spores) and aflatoxin holds promise for future development of anti-fungal therapeutics.

View Article: PubMed Central - PubMed

Affiliation: Department of Bacteriology and Department of Medical Microbiology and Immunology, 1550 Linden Drive, Madison, WI 53706, USA.

ABSTRACT
Oxylipins regulate Aspergillus development and mycotoxin production and are also involved in Aspergillus quorum sensing mechanisms. Despite extensive knowledge of how these oxylipins are synthesized and what processes they regulate, nothing is known about how these signals are detected and transmitted by the fungus. G protein-coupled receptors (GPCR) have been speculated to be involved as they are known oxylipin receptors in mammals, and many putative GPCRs have been identified in the Aspergilli. Here, we present evidence that oxylipins stimulate a burst in cAMP in A. nidulans, and that loss of an A. nidulans GPCR, gprD, prevents this cAMP accumulation. A. flavus undergoes an oxylipin-mediated developmental shift when grown at different densities, and this regulates spore, sclerotial and aflatoxin production. A. flavus encodes two putative GprD homologs, GprC and GprD, and we demonstrate here that they are required to transition to a high-density development state, as well as to respond to spent medium of a high-density culture. The finding of GPCRs that regulate production of survival structures (sclerotia), inoculum (spores) and aflatoxin holds promise for future development of anti-fungal therapeutics.

Show MeSH
Related in: MedlinePlus