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Differential gene expression drives cell-cycle-dependent transition from monopolar to bipolar growth in fission yeast

ABSTRACT: In S. pombe, cells transition from monopolar to bipolar growth in a cell cycle-dependent manner. To investigate this, we performed RNA-seq analysis of the cell-cycle mutant cdc10-129 to identify distinct gene expression patterns in G1 versus G2 phase. Our analysis identified upregulation of the pheromone- and stress-response pathways in G1/S-arrested cells and cell wall organization genes in G2 cells. Protein interaction networks identified a spk1-byr2-ste11 stress-response hub in G1/S. in agreement we find that cells spk1 are precociously bipolar. We propose that pheromone-response pathways block bipolarity until nutrient-rich conditions downregulate these pathways, enabling cell cycle progression and bipolar transition.

ORGANISM(S): Schizosaccharomyces pombe

PROVIDER: GSE326505 | GEO | 2026/03/31

REPOSITORIES: GEO

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Project description:We performed single-cell RNA sequencing of a lymphoma (OCI-Ly18) subcutaneous tumor harvested from NSG mice two weeks after infusion with CART19 plus DMSO or CART19 plus Venetoclax (Suppl. Fig. 3A). Lymphoma cells with shared gene expression profiles were clustered using uniform manifold and approximation (UMAP) analysis. We identified six clusters characterized by different cell-cycle phases (Suppl. Fig. 3B), including one G1-dominant cluster, two S clusters, one G1/G2 cluster, one G2/M cluster, and an M cluster with high Ki67 expression. First, we observed a substantially lower proportion of cells assigned to G1-dom in the CART19/venetoclax-treated condition (8.4%) than in the CART19-treated condition (24%). These indicated a prevalent depletion of the G1-dom cluster by the addition of venetoclax (Suppl. Fig. 4C). In accordance with recent reports that venetoclax can induce cell cycle arrest and death in tumor cells in G1 39, these results suggest that venetoclax treatment also enhances CART’s anti-tumor efficacy by hindering the progression of cell cycle. Interestingly, the “G1-dominant (G1-dom)” and the additional “MKI67hi” cluster (high proliferative cells) showed significant enrichment of genes corresponding to interferon-gamma responsiveness, suggesting that the cells of these two clusters might have been interacting with CART cells (Suppl. Fig. 4D). Of note, by performing GO enrichment analysis with differentially expressed genes (DEGs) between CART19 and CART19/venetoclax combination in the MKI67hi cluster that represent a rapidly proliferating tumor subpopulation, we identified several pathways, including enrichment of the negative regulation of the G2/M phase transition in the CART19/venetoclax-treatment condition in the MKI67hi cluster (Suppl. Fig. 4E and 4F). Taken together, these data implicate that venetoclax treatment enhances CART-mediated tumor killing by promoting tumor apoptosis and inhibiting the cell cycle in cancer cells while also enhancing the interferon responses in neoplastic B-cells when engaging CART cells.

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Differential gene expression drives cell-cycle-dependent transition from monopolar to bipolar growth in fission yeast

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