bioRxiv Science⌕ Search

Biology subjects

Peterson, A. F.

Publications and source records attributed to Peterson, A. F..

3 recordsLinked to original sources

Reconstructing the deep phylogeny of the MAPK signaling network: functional specialization via multi-tier coevolutionary expansion

The mitogen-activated protein kinase (MAPK) signaling network is a three-tier cascade that regulates key cellular responses in eukaryotes. However, the evolutionary origins of its complex interactions and functional diversity remain poorly understood. Here, we conducted a comprehensive phylogenetic analysis of MAPK components across Eukarya to delineate divergences of non-human orthologs of human paralogs along the human evolutionary backbone. We identified two major pulses of coevolutionary expansion: one predating the divergence of fungi and animals, and another predating the origin of animals. Our reconstruction also infers a polyphyletic origin for the atypical MAPKs. Integrating functional literature across eukaryotic taxa with our reconstructed trees reveals that the two clades of MAP3K, Sterile-like (STE) and tyrosine kinase-like (TKL), had distinct evolutionary trajectories and influences on downstream pathway diversification. STEs that function as MAP3Ks are conserved across extant eukaryotes. Despite the absence of TKL MAP3Ks in many early diverging eukaryotes, the expansion of TKL MAP3Ks aligns phylogenetically and functionally with that of the downstream MAP2Ks and MAPKs. We thus propose that the MAPK network originated as a STE-regulated pathway, and that subsequent radiations of the TKLs drove the diversification of downstream components and top-down finetuning of pathway specificity. We thus provide an evolutionary framework for generating novel hypotheses on the functional diversity of this key signaling network, including potential insights into the evolution of animal multicellularity. Our study demonstrates that phylogenetics can offer new perspectives towards understanding complex cellular physiology. SignificanceThe mitogen-activated protein kinase (MAPK) signaling network responds to various signals and regulates basic cell physiology including proliferation and apoptosis. This three-tier network is universal in eukaryotes, but there is great functional diversity among different homologs as well as different taxa. Here we compared amino acid sequences to reconstruct MAPK evolutionary history as a network. We found that the three levels expand in parallel, showcasing a special case of coevolution. Two distinct pulses of network expansion predate the origin of animals, indicating that the functional diversity of human MAPK network proteins originate from ancient evolutionary radiations. Together, our study provides a critical look at the deep history of this important network.

evolutionary biology↗

Non-catalytic role of phosphoinositide 3-kinase in mesenchymal cell migration through non-canonical induction of p85beta/AP-2-mediated endocytosis

Class IA phosphoinositide 3-kinase (PI3K) galvanizes fundamental cellular processes such as migration, proliferation, and differentiation. To enable multifaceted roles, the catalytic subunit p110 utilizes a multi- domain, regulatory subunit p85 through its inter SH2 domain (iSH2). In cell migration, their product PI(3,4,5)P3 generates locomotive activity. While non-catalytic roles are also implicated, underlying mechanisms and its relationship to PI(3,4,5)P3 signaling remain elusive. Here, we report that a disordered region of iSH2 contains previously uncharacterized AP-2 binding motifs which can trigger clathrin and dynamin-mediated endocytosis independent of PI3K catalytic activity. The AP-2 binding motif mutants of p85 aberrantly accumulate at focal adhesions and upregulate both velocity and persistency in fibroblast migration. We thus propose the dual functionality of PI3K in the control of cell motility, catalytic and non- catalytic, arising distinctly from juxtaposed regions within iSH2.

cell biology↗

Collective MAPK Signaling Dynamics Coordinates Epithelial Homeostasis

Epithelial tissues are constantly challenged by individual cell fate decisions while maintaining barrier function. During oncogenesis, mutant and normal cells also differ in their signaling states and cellular behaviors creating competitive interactions that are poorly understood. Here we show that the temporal patterns of MAPK activity are decoded by the ADAM17-EGFR paracrine signaling axis to coordinate migration of neighboring cells and promote extrusion of aberrantly-signaling cells. Concurrently, neighboring cells increase proliferation to maintain cell density while oncogene expressing cells undergo cell cycle arrest. Moreover, the stress MAPK p38 elicits the same paracrine signaling and extrusion response, suggesting that the ADAM17-EGFR pathway constitutes a quality control mechanism to eliminate and replace unfit cells from epithelial tissues. Overall, we show that the temporal patterns of MAPK activity coordinates both single and collective cell behaviors to maintain tissue homeostasis.

cell biology↗