期刊
JOURNAL OF FUNGI
卷 7, 期 11, 页码 -出版社
MDPI
DOI: 10.3390/jof7110920
关键词
Transient Receptor Potential (TRP); calcium; cell wall; Aspergillus nidulans
资金
- National Natural Science Foundation of China [31861133014, 31770086]
- Priority Academic Program Development (PAPD) of Jiangsu Higher Education Institutions
The putative TRP-like calcium channel trpR in the filamentous fungus Aspergillus nidulans plays important roles in conidiation and adapting to cell wall disruption reagents, especially under calcium-limited conditions. TrpR has an opposite response to the previously identified high-affinity calcium channels CchA/MidA in reacting to cell wall disruption reagents and regulating calcium transients. However, an addition of calcium can rescue the defects in TrpR and CchA/MidA, indicating calcium's ability to bypass the necessary requirement.
Transient Receptor Potential (TRP) proteins constitute a superfamily that encodes transmembrane ion channels with highly diverse permeation and gating properties. Filamentous fungi possess putative TRP channel-encoded genes, but their functions remain elusive. Here, we report that a putative TRP-like calcium channel, trpR, in the filamentous fungus Aspergillus nidulans, performs important roles in conidiation and in adapting to cell wall disruption reagents in a high temperature-induced defect-dependent manner, especially under a calcium-limited culture condition. The genetic and functional relationship between TrpR and the previously identified high-affinity calcium channels CchA/MidA indicates that TrpR has an opposite response to CchA/MidA when reacting to cell wall disruption reagents and in regulating calcium transients. However, a considerable addition of calcium can rescue all the defects that occur in TrpR and CchA/MidA, meaning that calcium is able to bypass the necessary requirement. Nevertheless, the colocalization at the membrane of the Golgi for TrpR and the P-type Golgi Ca2+ ATPase PmrA suggests two channels that may work as ion transporters, transferring Ca2+ from the cytosol into the Golgi apparatus and maintaining cellular calcium homeostasis. Therefore, combined with data for the trpR deletion mutant revealing abnormal cell wall structures, TrpR works as a Golgi membrane calcium ion channel that involves cell wall integration.
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