Search bioRxiv⌕ Search

bioRxiv · 10.1101/2025.09.25.678408

A Daily Cycle of White Collar Complex Dephosphorylation Sustains Circadian Rhythmicity in Neurospora

Abstract

As a photoreceptor, the transcription factor complex WCC acutely activates [~]5% of the genome in response to blue light, while as the circadian positive element in the dark WCC influences expression of about 40% of the transcriptome. Among WCC-regulated genes is frq which is both acutely light-activated through a pLRE and circadian-regulated through a C-box promoter element that is not active in constant light. The complex of FRQ, FRH, and CK1, the FFC, phosphorylates WCC at >95 sites, thereby repressing its activity and closing the circadian feedback loop in the dark. Although FFC has no described role in the light, we validated the expectation that FFC-driven WCC phosphorylation also silences C-box promoters in constant light, thereby confirming two classes of WCC targets, C-box-like that are normally repressed in the light and pLRE-like that remain light-active despite FFC-driven WCC phosphorylation. Genome-wide derepression of C-box-like promoters in frq-null fungi may explain reported non-circadian effects seen in some frq-null fungi including reduced virulence and conidiation. Reanalysis of WCC-mediated circadian activation and repression revealed that, while at dusk most WCC is phosphorylated and repressed, subsequent circadian activation is the result of transient dephosphorylation/derepression of just a small subset of this WCC pool; this small active pool drives expression of FRQ, nucleating the FFC, which rapidly re-phosphorylates the WCC pool to repress it, a phosphorylation/dephosphorylation cycle that can run for days without new WCC synthesis. The realization that both FFC and WCC are regulated primarily through phosphorylation rather than turnover leaves the circadian oscillator looking much like a phoscillator, emphasizing the primacy of post-translational regulation in timekeeping. SignificanceAt the core of circadian clocks of fungi and animals, a protein heterodimer drives expression of gene(s) whose products inactivate the heterodimer via phosphorylation. To sustain the cycle through multiple days, the activity of the heterodimer must be restored, but the means through which this happens have been unclear. In the clock model Neurospora, the White Collar Complex (WCC) is the heterodimer and FFC is the complex that inactivates it. We determined that WCC activity is restored principally by removal of the inhibitory phosphorylations and that for at least several days no new synthesis of WCC is required. The results confirm the existence of a large pool of inactive WCC in the cell and highlights the delicate balance between FCC-dependent phosphorylation/inactivation and phosphatase-dependent dephosphorylation/reactivation. Each morning, this balance allows transient activation of a fraction of the inactive WCC pool, thereby restarting the circadian cycle.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Wang, B., Zhou, X., Loros, J. J., Dunlap, J. C.. 2025-09-26. A Daily Cycle of White Collar Complex Dephosphorylation Sustains Circadian Rhythmicity in Neurospora. https://doi.org/10.1101/2025.09.25.678408

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

KEEP EXPLORING

Related preprints

Conjunctive Targeting Links Drug Synergy to Emergent Proteome Structural States

Combinatorial therapies are widely used in the treatment of acute myeloid leukemia (AML) to address disease heterogeneity, adaptive resistance, and rewired signaling and metabolic states. Yet drug prioritization remains largely guided by clinical or phenotypic evidence, while the molecular mechanisms underlying effective drug combinations remain incompletely defined. To narrow this gap, we developed Combinatorial high-ratio Partial proteolysis with reference PRoteome Analysis (CoPPRA), a structural proteomics workflow based on limited proteolysis of cell lysates that profiles drug-associated changes in regional protein accessibility at peptide-level resolution. Here, we applied CoPPRA to ruxolitinib and ulixertinib, individually and in combination, in AML-related cell lysates. Our findings extend conjunctive targeting (CT), a recently proposed mechanism of combinatorial drug action in which combined exposure produces protein targeting patterns not observed with either drug alone. Previously identified through combination-associated changes in protein solubility/stability, CT is examined here at peptide-level resolution through regional differences in proteolytic accessibility. The ruxolitinib-ulixertinib combination produced broad peptide-level accessibility changes, including a subset meeting the predefined criteria for CT. CT candidates predominantly exhibited regional accessibility changes, with altered peptide regions occurring against comparatively small changes across the remaining quantified peptides from the same proteins. MAP2K1 and ATP6V1G1 showed pronounced differences between overlapping peptide sequences, highlighting localized variation in combination-associated accessibility, including an ATP6V1G1 peptide mapping to an annotated helical region. Combination-associated increases in peptide signals were also observed in PIK3R1, BRD4, and PTPN11, linking regional accessibility changes to signaling and transcriptional regulators relevant to AML. Functional enrichment and network analyses further implicated nucleotide and glucose metabolism, ficolin-1-rich granules, ribosome-associated processes, and phagocytic vesicles. These results extend conjunctive targeting from protein-level solubility/stability changes to regional differences in proteolytic accessibility, showing that combination-associated effects can be concentrated within specific peptide regions rather than distributed uniformly across proteins. More broadly, CoPPRA provides a peptide-resolved approach for investigating the molecular features of combinatorial drug action and prioritizing protein regions for subsequent mechanistic validation.

biochemistry↗

Structural and biochemical characterisation of an iterative GCN5-related N-acetyltransferase required for fungal siderophore tailoring

Siderophore-mediated iron acquisition is essential for fungal survival, particularly under iron-limiting conditions. In Aspergillus fumigatus, SidG, a member of the GCN5-related N-acetyltransferase (GNAT) superfamily, catalyses the final step in the biosynthesis of the extracellular siderophore triacetylfusarinine C (TAFC) through sequential acetylation of the precursor fusarinine C (FsC). However, the timing, catalytic mechanism, and functional significance of this modification are not fully understood. Here, we reconstituted SidG activity in vitro and combined native mass spectrometry, X-ray crystallography, molecular dynamics simulations, and site-directed mutagenesis to investigate its catalytic properties. Our analyses demonstrate that SidG selectively binds acetyl-CoA from the cellular milieu and iteratively acetylates the FsC scaffold prior to iron chelation. Structural, biochemical, and molecular dynamics analyses support a direct transfer mechanism, identify key catalytic residues, and demonstrate the strict selectivity of SidG for short-chain acyl-CoA donors. Together, these findings establish the molecular basis for SidG-dependent siderophore tailoring and expand our understanding of GNAT-catalysed transformations in fungal natural product biosynthesis.

biochemistry↗

Reconstitution of +1 nucleosome transcription reveals coordinated functions of SAGA, Mediator, and TFIIH

The +1 nucleosome has emerged as a key regulator of eukaryotic transcription, but how it controls transcription initiation remains poorly understood. Here we reconstitute transcription through the +1 nucleosome using eleven purified yeast factors: RNA polymerase II (Pol II), the six general transcription factors (GTFs), TFIIS, the activator Pho4, and the SAGA and Mediator complexes. The system recapitulates key features of regulation observed in vivo. SAGA, acting with Pho4, directs pre-initiation complex (PIC) assembly to the correct position through its TBP-loading activity. Mediator stimulates transcription when the +1 nucleosome imposes a barrier to PIC formation, consistent with stabilization of productive TFIIH-DNA engagement. Contrary to the prevailing model, SAGA remains bound to the PIC after TBP loading and acetylates the +1 nucleosome within the assembled complex. The isolated PIC-Mediator-SAGA-nucleosome complex is transcriptionally active, and the repressive effect of the nucleosome is relieved by the DNA translocase activity of Ssl2, the TFIIH subunit that opens promoter DNA. TFIIH thus couples promoter melting to remodeling of the +1 nucleosome.

biochemistry↗