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Regulation of symbiotic interactions and primitive lichen differentiation by UMP1 MAP kinase in Umbilicaria muhlenbergii.

ABSTRACT: Lichens are of great ecological importance but mechanisms regulating lichen symbiosis are not clear. Umbilicaria muhlenbergii is a lichen-forming fungus amenable to molecular manipulations and dimorphic. Here, we established conditions conducive to symbiotic interactions and lichen differentiation and showed the importance of UMP1 MAP kinase in lichen development. In the initial biofilm-like symbiotic complexes, algal cells were interwoven with pseudohyphae covered with extracellular matrix. After longer incubation, fungal-algal complexes further differentiated into primitive lichen thalli with a melanized cortex-like and pseudoparenchyma-like tissues containing photoactive algal cells. Mutants deleted of UMP1 were blocked in pseudohyphal growth and development of biofilm-like complexes and primitive lichens. Invasion of dividing mother cells that contributes to algal layer organization in lichens was not observed in the ump1 mutant. Overall, these results showed regulatory roles of UMP1 in symbiotic interactions and lichen development and suitability of U. muhlenbergii as a model for studying lichen symbiosis.

SUBMITTER: Wang Y

PROVIDER: S-EPMC10620189 | biostudies-literature | 2023 Nov

REPOSITORIES: biostudies-literature

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Regulation of symbiotic interactions and primitive lichen differentiation by UMP1 MAP kinase in Umbilicaria muhlenbergii.

Wang Yanyan Y Li Rong R Wang Diwen D Qian Ben B Bian Zhuyun Z Wei Jiangchun J Wei Xinli X Xu Jin-Rong JR

Nature communications 20231101 1

Lichens are of great ecological importance but mechanisms regulating lichen symbiosis are not clear. Umbilicaria muhlenbergii is a lichen-forming fungus amenable to molecular manipulations and dimorphic. Here, we established conditions conducive to symbiotic interactions and lichen differentiation and showed the importance of UMP1 MAP kinase in lichen development. In the initial biofilm-like symbiotic complexes, algal cells were interwoven with pseudohyphae covered with extracellular matrix. Aft ...[more]

PMID: 37914724

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Project description:BackgroundConventional p38α inhibitors have limited efficacy in rheumatoid arthritis, possibly because p38 blockade suppresses the counter-regulatory mechanisms that limit inflammation. In contrast, targeting the upstream MAP kinase kinases, MKK3 and MKK6, partially maintains p38-mediated anti-inflammatory responses in bone marrow-derived macrophages (BMDM). In this study, we explored the mechanisms that preserve anti-inflammatory gene expression by evaluating differential regulation of IL-10 and p38-dependent anti-inflammatory genes in MKK3-/-, MKK6-/-, and p38 inhibitor-treated wildtype cells.MethodsBMDM from wild type (WT), MKK3-/-, and MKK6-/- mice were pre-treated with p38 inhibitor SB203580 (SB), JNK inhibitor SP600125 (SP), and/or ERK inhibitor PD98059 (PD) and stimulated with LPS. Supernatant protein levels were measured by multiplex bead immunoassay. mRNA expression was determined by qPCR and protein expression by Western blot analysis. De novo IL-10 mRNA synthesis was quantified in cells treated with ethynyl-uridine and LPS followed by reverse transcription and qPCR. mRNA half-life was measured in LPS-treated cells that were then incubated with actinomycin D ± SB203580.ResultsPre-treatment of WT BMDM with p38 inhibitor significantly reduced IL-10 production in the three groups, while ERK and JNK inhibitors had minimal effects. IL-10 production was significantly decreased in MKK3-/- BMDM compared with either WT or MKK6-/- cells. IL-10 mRNA expression was modestly reduced in MKK3-/- BMDM but was preserved in MKK6-/- cells compared with WT. De novo IL-10 mRNA synthesis was inhibited in MKK3-/- and p38 inhibitor pre-treated cells, but not MKK6-/- cells compared with WT. IL-10 mRNA half-life was markedly reduced in p38 inhibitor-treated WT cells while MKK-deficiency had minimal effect. DUSP1 mRNA levels were preserved in MKK-deficient cells but not in p38 inhibitor-treated WT cells. Tristetraprolin mRNA and protein levels were reduced in p38 inhibitor-treated WT cells compared with MKK6-/- cells.ConclusionUnlike p38-inhibition, the absence of MKK6 mostly preserves IL-10 and TTP protein expression in BMDM. MKK6-deficiency also spares DUSP1 and IL-1RA, which are key negative regulators of the inflammatory response. Together, these data suggest that MKK6 is a potential therapeutic target in RA.

Dataset Information

Regulation of symbiotic interactions and primitive lichen differentiation by UMP1 MAP kinase in Umbilicaria muhlenbergii.

Publications

Regulation of symbiotic interactions and primitive lichen differentiation by UMP1 MAP kinase in Umbilicaria muhlenbergii.

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