Highlights d BubR1 kinase activity is dispensable for the timing and progression of mitosis d BubR1 kinase-dead mutants have attenuated insulin signaling d Loss of BubR1 kinase activity compromises the homeostasis of tissue stem cells

Mitosis and endocytosis are two fundamental cellular processes essential for maintaining a eukaryotic life. Mitosis partitions duplicated chromatin enveloped in the nuclear membrane into two new cells, whereas endocytosis takes in extracellular substances through membrane invagination. These two processes are spatiotemporally separated and seemingly unrelated. However, recent studies have uncovered that endocytic proteins have moonlighting functions in mitosis, and mitotic complexes manifest additional roles in endocytosis. In this review, we summarize important proteins or protein complexes that participate in both processes, compare their mechanism of action, and discuss the rationale behind this multifunctionality. We also speculate on the possible origin of the functional reciprocity from an evolutionary perspective. An introduction to mitosis and endocytic pathwaysEukaryotic cells rely on endocytosis to uptake extracellular materials and their own plasma membrane components, in order to maintain homeostasis and respond to the varying environment [1-3]; they use the process of mitosis to achieve self-duplication and cell fate specification when differentiating [1,4]. These two Abbreviations AP2, adaptor protein-2; APC/C, anaphase-promoting complex/cyclosome; CCP, clathrin-coated pit; CCV, clathrin-coated vesicle; CHC, clathrin heavy chains; ch-TOG, colonic and hepatic tumor overexpressed gene; CLC, clathrin light chain; CME, clathrin-mediated endocytosis; CPC, chromosome passenger complex;

Human health is facing a host of new threats linked to unbalanced diets, including high sugar diet (HSD), which contributes to the development of both metabolic and behavioral disorders. Studies have shown that diet-induced metabolic dysfunctions can transmit to multiple generations of offspring and exert long-lasting health burden. Meanwhile, whether and how diet-induced behavioral abnormalities can be transmitted to the offspring remain largely unclear. Here, we showed that ancestral HSD exposure suppressed sweet sensitivity and feeding behavior in the offspring in Drosophila. These behavioral deficits were transmitted through the maternal germline and companied by the enhancement of H3K27me3 modifications. PCL-PRC2 complex, a major driver of H3K27 trimethylation, was upregulated by ancestral HSD exposure, and disrupting its activity eliminated the transgenerational inheritance of sweet sensitivity and feeding behavior deficits. Elevated H3K27me3 inhibited the expression of a transcriptional factor Cad and suppressed sweet sensitivity of the sweet-sensing gustatory neurons, reshaping the sweet perception and feeding behavior of the offspring. Taken together, we uncovered a novel molecular mechanism underlying behavioral abnormalities across multiple generations of offspring upon ancestral HSD exposure, which would contribute to the further understanding of long-term health risk of unbalanced diet.

We discovered an anomalous effect of the aging degree on the ionic permeability of colloidal silica.

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