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February 25, 2026Molecular and Cellular Biology2 citations

p62 Coordinates Autophagy, cAMP Signalling, and Cell-Fate Determination in Dictyostelium discoideum

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SGSaksham GautamSSShweta Saran

Key Points

  • The research investigates the role of p62 in autophagy and cell-fate decisions in Dictyostelium discoideum.
  • Analyzed the effects of p62 deletion on development and autophagy in Dictyostelium discoideum
  • Measured levels of intracellular glucose, cAMP, and autophagic flux
  • Performed rescue experiments with exogenous cAMP in p62 null cells
  • Assessed cell differentiation and lineage decisions through p62 manipulation
  • Loss of p62 resulted in altered levels of glucose, cAMP, and ubiquitinated proteins
  • Impaired cell aggregation and fruiting body formation were observed in p62 null cells
  • Exogenous cAMP treatment partially rescued developmental defects in p62 null cells
  • Deletion of p62 biased cells toward pre-spore differentiation, while overexpression favored pre-stalk lineage
  • p62 modulated autophagic flux by regulating AMPK levels and cAMP dynamics

Abstract

p62/SQSTM1 is a multifunctional adaptor protein playing a central role in the regulation of autophagy and stress response pathways in higher eukaryotes. However, its functional relevance in lower eukaryotes like Dictyostelium remains largely unexplored. In this study, we demonstrate that Dictyostelium p62 is crucial for cAMP-mediated development and autophagy. Loss of p62 alters levels of intracellular glucose, cAMP, ubiquitinated proteins and autophagic flux. These defects result in impaired cell aggregation and abnormal fruiting body formation, accompanied by reduced spore viability. Interestingly, pulsing of p62 null cells with exogenous cAMP could partially rescue the developmental defects, implicating a role of p62 in maintaining the intracellular cAMP levels required for starvation stress-induced development. p62 also influences cell-fate decisions during development as its deletion biases cells toward pre-spore differentiation, whereas overexpression promotes pre-stalk lineage. Mechanistically, p62 also modulates autophagy flux potentially via regulating AMPK levels along with cAMP dynamics. Together, these findings position p62 as an evolutionarily conserved key adaptor protein that provides new insights into the molecular mechanisms underlying multicellular development.

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Cite This Study

Gautam et al. (2026) studied this question.

synapsesocial.com/papers/699e9152f5123be5ed04ec56https://doi.org/10.1080/10985549.2026.2627237
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