Search bioRxiv⌕ Search

bioRxiv · 10.64898/2026.08.19.745713

Species Context Reverses PPIP5K Control of Fungal Morphogenesis and Actin Organization

Abstract

Inositol pyrophosphates are conserved signaling molecules synthesized by the bifunctional PPIP5K enzymes, but how their cellular functions diversify across species remains poorly understood. Here, we compared the PPIP5K enzyme Asp1 in the fission yeasts Schizosaccharomyces pombe and Schizosaccharomyces japonicus and in the distantly related fungus Ustilago maydis. All three homologs retained a conserved kinase-phosphatase architecture and catalytic activity. However, whereas Asp1 produced broadly similar effects on actin organization and morphogenesis in S. pombe and U. maydis, its regulatory output was reversed in S. japonicus. In S. pombe and U. maydis, Asp1 positively supported Arp2/3-dependent actin functions, as loss of Asp1 increased sensitivity to the Arp2/3 inhibitor CK666. In contrast, deletion of asp1 in S. japonicus conferred strong CK666 resistance and caused excessive, spatially deregulated actin-patch organization. This opposing cytoskeletal phenotype was mirrored at the level of morphogenesis: Asp1 restricted the yeast-to-hypha transition in S. japonicus, whereas Asp1 was required for pseudohyphal growth in S. pombe and for filamentous development in U. maydis. However, the negative regulatory activity observed in S. japonicus was not an intrinsic property of the SjAsp1 protein. When expressed in S. pombe, SjAsp1 promoted invasive pseudohyphal growth, reproducing the regulatory output of the S. pombe Asp1 morphogenesis pathway rather than that of its native species. Similarly, SjAsp1 supported Arp2/3 functions when expressed in S. pombe. Thus, SjAsp1 adopted the functional behavior imposed by the host cellular environment. S. pombe Asp1 was originally identified as a suppressor of Arp2/3-complex mutant phenotypes, establishing a genetic connection between Asp1 and the actin nucleator. Extending this link, affinity enrichment with inositol pyrophosphates reagents recovered all seven subunits of the S. pombe Arp2/3 complex, providing biochemical support for a potential association between inositol pyrophosphate and Arp2/3. Together, these findings identify S. japonicus as a functional outlier in which a conserved PPIP5K pathway produces an opposing biological output. They further demonstrate that this divergence is determined primarily by species-specific cellular networks rather than by intrinsic differences in the Asp1 protein.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Fleig, U., Koc, E., Juhran, L., Emmerich, V., Alcazar-Roman, A. R., Bartsch, S. M., Saiardi, A., van Wijlick, L., Postma, J., Lenz, T., Fiedler, D., Feldbruegge, M., Stuehler, K., Span, I.. 2026-08-20. Species Context Reverses PPIP5K Control of Fungal Morphogenesis and Actin Organization. https://doi.org/10.64898/2026.08.19.745713

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Contact-phagy remodels ER-mitochondria contact sites

Membrane contact sites between the endoplasmic reticulum (ER) and other organelles coordinate cellular organization, metabolism and stress responses, yet how these interfaces are selectively remodeled and removed remains poorly understood. Here we identify a selective autophagy pathway that targets defined ER-mitochondria contact-site (ERMCS) subdomains for turnover, a process we term Contact-phagy. The ER-resident chaperone SIGMAR1 forms a functional complex with the ER-phagy receptor CCPG1, and SIGMAR1-CCPG1 nanoclusters define ERMCS-associated sites of autophagy initiation. Contact-phagy is selectively engaged by metabolic and mitochondrial stress and promotes turnover of defined contact-site components without broadly affecting general ER-phagy, mitophagy or bulk autophagy. At these sites, SIGMAR1-CCPG1 function is coupled to mitochondrial fission: MFF promotes DRP1 recruitment to ERMCS, whereas loss of CCPG1 or SIGMAR1 causes abnormal persistence and clustering of DRP1 and MFF, accompanied by altered mitochondrial remodeling. Loss of CCPG1 further disrupts ER-mitochondria organization and mitochondrial function in pancreatic tissue, while pancreatic cancer cells depend on CCPG1 and SIGMAR1 for organelle integrity and bioenergetic capacity. Together, our findings establish Contact-phagy as a selective pathway for the turnover of defined organelle contact site subdomains and suggest a broader principle by which interorganelle interfaces are maintained.

cell biology↗

HUH-tag conjugation enables accessible, site-specific functionalization of DNA origami with signaling-competent proteins

DNA origami enables precise nanometer scale control over the number, spacing, and geometry of biomolecules, making it a powerful tool for dissecting spatially organized biological processes such as receptor signaling. However, functionalizing origami with proteins remains a bottleneck restricting the technology to specialized laboratories. Here we show that viral-derived HUH endonuclease tags, small (~10 kDa) domains that form a covalent phosphotyrosine bond with short unmodified ssDNA, provide a simple and cost-effective route to decorating DNA origami with functional proteins. Using interleukin-1{beta} (IL-1{beta}) as a model ligand, we generated recombinant IL-1{beta}-HUH, achieved efficient site-specific conjugation to unmodified ssDNA within minutes, and coupled the conjugates to a DNA origami pegboard with tunable stoichiometry. IL-1{beta}-functionalized origami triggered ligand-dependent signalling in living cells and allowed visualization of the recruitment of downstream signaling molecules, confirming that HUH-tag conjugation preserves functionality. Because this strategy requires only standard molecular biology equipment and unmodified DNA, it lowers a technical and financial barrier to DNA origami-based experimentation, opening the approach to a broader range of biological questions and laboratories outside the DNA nanotechnology field.

cell biology↗

Multivalent BBSome-IFT proximities support IFT-A-IFT-B coordination in vivo

Intraflagellar transport (IFT) depends on coordinated movement of IFT-A and IFT-B, yet how these assemblies remain coupled within dynamic ciliary trains is unclear. Here, we combine endogenous fluorescent knock-in tagging, quantitative in vivo FLIM-FRET, structural modeling, and targeted mutagenesis to define IFT organization in C. elegans and mammalian cells. FLIM-FRET mapping identifies proximity networks within IFT-B and places IFT144 near IFT172 and IFT88 in intact cilia. Loss of BBSome function is associated with weaker IFT-A-IFT-B proximity signals and divergent subcomplex transport dynamics, consistent with a contribution of the BBSome to IFT coordination in vivo. Split-GFP complementation places BBSome components near IFT-A and IFT-B, while structural modeling nominates complementary charged surfaces on the IFT46-IFT52 dimer and BBS7/BBS9. Charge-reversal mutations targeting these surfaces impair BBSome recruitment and functional rescue. Together, these findings support a model in which multivalent BBSome-IFT proximities contribute to IFT-A-IFT-B coordination during ciliary transport.

cell biology↗