Kazuki Mochizuki

Cellular memory, or epigenetic memory, represents the capacity for cells to retain information beyond the underlying DNA sequence. This heritable characteristic is primarily governed by epigenetic mechanisms which enable cells to maintain specialized characteristics across divisions. This persistent cellular state is essential for fundamental biological processes, such as maintaining tissue identity and facilitating cell differentiation, especially embryonic cells. Early-stage perturbations such as assisted reproductive technologies (ART) and nutritional stress links embryonic exposures to adult health and disease within the Developmental Origins of Health and Disease (DOHaD) framework. Crucially, memory established during early embryogenesis links these epigenetic modifications to adult long-term phenotypes related to metabolic disorders. These modifications—including DNA methylation, histone modifications, and non-coding RNAs—support cellular memory transmission across cell divisions, and in certain organisms, can be transmitted across generations without alterations to the DNA sequence. This review synthesizes recent advances in epigenetic pathways that mediate cellular memory, highlights critical preimplantation windows of vulnerability and outlines gaps necessary for mammalian developing interventions that safeguard future generations.

The development of steatosis due to early complete weaning in mice is closely positively associated with a reduced amount of PC and related metabolites, transcriptome changes including Pemt, and alterations in histone modifications around Pemt.

The present study investigates nitrogen (N) flows within the food system of Yamanashi Prefecture from 2000 to 2015, by longitudinally integrating Input–Output analyses with N flow models. By unveiling detailed N flows specifically in the food manufacturing sector (food processing, distribution, and food service), this study aims to analyse the recyclability of N losses quantitatively. Results showed approximately 60% of the total N input resulted in N loss. The N losses can be classified into highly recyclable nitrogen (high-RAN: 11%), low-recyclable nitrogen (low-RAN: 16%) and non-recyclable nitrogen (non-RAN: 73%). A comparative analysis was performed with three scenarios according to the Green Food System Strategy: a control scenario of 2050, Scenario l targeting chemical fertilizer reduction, and Scenario 2 targeting chemical fertilizer reduction and increased feed self-sufficiency. Compared to the control, both Scenario 1 and Scenario 2 demonstrated improvements in N recycling efficiencies by 4.9% and 15.0%, respectively. Notably, the Scenario 2, which separately reutilised high-RAN and low-RAN, expanded the N demand for recycling, achieving a 6.4% enhanced N loss reduction compared to the Scenario 1. In conclusion, this study provides the suggestion that the sophistication of the reutilisation network can promote the reduction of N losses.

Recently, we have demonstrated that mice, cultured embryos in α-minimum essential medium (αMEM) and subsequent fed a high-fat, high-sugar diet, developed steatohepatitis. In this study, we investigated using these samples whether the expression of lipid droplet formation genes in the liver is higher in MEM mice, whether these expressions are regulated by histone acetylation, writers/readers of histone acetylation, and the transcriptional factors of endoplasmic reticulum stress. Mice were produced by two-cell embryos in αMEM or standard potassium simplex-optimized medium (control) in vitro for 48 h, and implanted into an oviduct for spontaneous delivery. MEM and control-mice were fed a high-fat, high-sugar diet for 18 wk, and then liver samples were collected and analyzed by histology, qRT-PCR, and chromatin immunoprecipitation assay. Gene expression of Cidea, Cidec, and Plin4 were higher in MEM mice and histone H3K9 acetylation, BRD4, and CBP were higher in MEM mice than in control mice around those genes. However, the binding of endoplasmic reticulum stress-related transcription factors (ATF4, CHOP and C/EBPα) around those genes in the liver, was not clearly differed between MEM mice and control mice. The increased expression of Cidea, Cidec and Plin4 in the liver, accompanied by the development of steatohepatitis in mice induced is positively associated with increased histone H3K9 acetylation and CBP and BRD4 binding around these genes.