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Genome architecture and selective signals compensatorily shape plastic response to a new environment.

ABSTRACT: Transcriptional plasticity interacts with natural selection in complex ways and is crucial for the survival of species under rapid climate change. How 3D genome architecture affects transcriptional plasticity and its interaction with genetic adaptation are unclear. We transplanted estuarine oysters to a new environment and found that genes located in active chromatin regions exhibited greater transcriptional plasticity, and changes in these regions were negatively correlated with selective signals. This indicates a trade-off between 3D active regions and selective signals in shaping plastic responses to a new environment. Specifically, a mutation, lincRNA, and changes in the accessibility of a distal enhancer potentially affect its interaction with the ManⅡa gene, which regulates the muscle function and survival of oysters. Our findings reveal that 3D genome architecture compensates for the role of genetic adaptation in environmental response to new environments and provide insights into synergetic genetic and epigenetic interactions critical for fitness-related trait and survival in a model marine species.

SUBMITTER: Li A

PROVIDER: S-EPMC10362523 | biostudies-literature | 2023 Jul

REPOSITORIES: biostudies-literature

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Genome architecture and selective signals compensatorily shape plastic response to a new environment.

Li Ao A Zhao Mingjie M Zhang Ziyan Z Wang Chaogang C Zhang Kexin K Zhang Xu X De Wit Pierre Raoul PR Wang Wei W Gao Juntao J Guo Ximing X Zhang Guofan G Li Li L

Innovation (Cambridge (Mass.)) 20230621 4

Transcriptional plasticity interacts with natural selection in complex ways and is crucial for the survival of species under rapid climate change. How 3D genome architecture affects transcriptional plasticity and its interaction with genetic adaptation are unclear. We transplanted estuarine oysters to a new environment and found that genes located in active chromatin regions exhibited greater transcriptional plasticity, and changes in these regions were negatively correlated with selective signa ...[more]

PMID: 37485076

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Project description:BackgroundMicroglia are resident myeloid cells of the central nervous system (CNS) that are maintained by self-renewal and actively participate in tissue homeostasis and immune defense. Under the influence of endogenous or pathological signals, microglia undertake biochemical transformations that are schematically classified as the pro-inflammatory M1 phenotype and the alternatively activated M2 state. Dysregulated proliferation of M1-activated microglia has detrimental effects, while an increased number of microglia with the alternative, pro-resolving phenotype might be beneficial in brain pathologies; however, the proliferative response of microglia to M2 signals is not yet known. We thus evaluated the ability of interleukin-4 (IL-4), a typical M2 and proliferative signal for peripheral macrophages, to induce microglia proliferation and compared it with other proliferative and M2 polarizing stimuli for macrophages, namely colony-stimulating factor-1 (CSF-1) and the estrogen hormone, 17β-estradiol (E2).MethodsRecombinant IL-4 was delivered to the brain of adult mice by intracerebroventricular (i.c.v.) injection; whole brain areas or ex vivo-sorted microglia were analyzed by real-time PCR for assessing the mRNA levels of genes related with cell proliferation (Ki67, CDK-1, and CcnB2) and M2 polarization (Arg1, Fizz1, Ym-1) or by FACS analyses of in vivo BrdU incorporation in microglia. Primary cultures of microglia and astrocytes were also tested for proliferative effects.ResultsOur results show that IL-4 only slightly modified the expression of cell cycle-related genes in some brain areas but not in microglia, where it strongly enhanced M2 gene expression; on the contrary, brain delivery of CSF-1 triggered proliferation as well as M2 polarization of microglia both in vivo and in vitro. Similar to IL-4, the systemic E2 administration failed to induce microglia proliferation while it increased M2 gene expression.ConclusionsOur data show that, in contrast to the wider responsiveness of peripheral macrophages, microglia proliferation is stimulated by selected M2 polarizing stimuli suggesting a role for the local microenvironment and developmental origin of tissue macrophages in regulating self-renewal following alternative activating stimuli.

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Genome architecture and selective signals compensatorily shape plastic response to a new environment.

Publications

Genome architecture and selective signals compensatorily shape plastic response to a new environment.

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