A conserved Foxp1-Pde4d axis regulates inflammatory responsiveness

Foxp1 positively regulates Pde4d expression, and this Foxp1–Pde4d coupling is conserved across vertebrate tissues and damage models, shaping inflammatory responsiveness.

• Why it matters: Inflammatory programs vary even under the same insult, but the conserved regulators that set a cell’s later response capacity are unclear.
• What they did: In adipocyte progenitors under genotoxic stress, transcriptome-wide analysis linked lower IFN and higher NF{kappa}B programs to Foxp1 and Pde4d; ChIP-seq showed reduced Foxp1 occupancy at a Pde4d element, and Foxp1 gain/loss experiments established Foxp1 as a positive regulator of Pde4d.
• The result: In zebrafish, Foxp1 loss increased basal NF{kappa}B activity but blunted injury-induced NF{kappa}B activation and impaired macrophage recruitment; adenylyl cyclase inhibition restored recruitment, linking the phenotype to cAMP signaling.

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