Heme Oxygenase/Carbon Monoxide Participates in the Regulation of <i>Ganoderma lucidum</i> Heat-Stress Response, Ganoderic Acid Biosynthesis, and Cell-Wall Integrity
Carbon monoxide (CO), a product of organic oxidation processes, arises in vivo principally from the enzymatic reaction of heme oxygenase (HO, transcription gene named <i>HMX1</i>). HO/CO has been found to exert many salutary effects in multiple biological processes, including the stress...
| Main Authors: | , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
MDPI AG
2022-10-01
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| Series: | International Journal of Molecular Sciences |
| Subjects: | |
| Online Access: | https://www.mdpi.com/1422-0067/23/21/13147 |
| Summary: | Carbon monoxide (CO), a product of organic oxidation processes, arises in vivo principally from the enzymatic reaction of heme oxygenase (HO, transcription gene named <i>HMX1</i>). HO/CO has been found to exert many salutary effects in multiple biological processes, including the stress response. However, whether HO/CO is involved in the regulation of the heat-stress (HS) response of <i>Ganoderma lucidum</i> (<i>G. lucidum</i>) is still poorly understood. In this paper, we reported that under heat stress, the <i>HMX1</i> transcription level, HO enzyme activity, and CO content increased by 5.2-fold, 6.5-fold and 2-fold, respectively. <i>HMX1</i> silenced strains showed a 12% increase in ganoderic acid (GA) content under HS as analyzed by HPLC. Furthermore, according to Western blot analysis of the protein phosphorylation levels, <i>HMX1</i> attenuated the increase in phosphorylation levels of slt2, but the phosphorylation levels were prolonged over a 3 h HS time period. The chitin and glucan content in <i>HMX1</i> silenced strains increased by 108% and 75%, respectively. In summary, these findings showed that the HO/CO system responds to heat stress and then regulates the HS-induced GA biosynthesis and the cell-wall integrity mediated by the Slt-MAPK phosphorylation level in <i>G. lucidum</i>. |
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| ISSN: | 1661-6596 1422-0067 |