Food Science of Animal Resources (Food Sci. Anim. Resour.) is an international, peer-reviewed bimonthly journal publishing original research and reviews on basic and applied aspects of the use of animal resources including the meat, egg, dairy, and edible insect/worm products. Food Sci. Anim. Resour. is published and distributed by the Korean Society for Food Science of Animal Resources.

Assisted reproductive technologies (ARTs) have developed considerably in recent years; however, they cannot rectify germ cell aplasia, such as non-obstructive azoospermia (NOA) and oocyte maturation failure syndrome. In vitro gametogenesis is a promising technology to overcome infertility, particularly germ cell aplasia. Early germ cells, such as primordial germ cells, can be relatively easily derived from pluripotent stem cells (PSCs); however, further progression to post-meiotic germ cells usually requires a gonadal niche and signals from gonadal somatic cells. Here, we review the recent advances in in vitro male and female germ cell derivation from PSCs and discuss how this technique is used to understand the biological mechanism of gamete development and gain insight into its application in infertility.

Mitochondria are crucial for cellular energy metabolism and are involved in signaling, aging, and cell death. They undergo dynamic changes through fusion and fission to adapt to different cellular states. In this study, we investigated the effect of knocking out the dynamin 1-like protein (Dnm1l) gene, a key regulator of mitochondrial fission, in neural stem cells (NSCs) differentiated from Dnm1l knockout embryonic stem cells (Dnm1l^−/− ESCs). Dnm1l^−/− ESC-derived NSCs (Dnm1l^−/− NSCs) exhibited similar morphology and NSC marker expression (Sox2, Nestin, and Pax6) to brain-derived NSCs, but lower Nestin and Pax6 expression than both wild-type ESC-derived NSCs (WT-NSCs) and brain-derived NSCs. In addition, compared with WT-NSCs, Dnm1l^−/− NSCs exhibited distinct mitochondrial morphology and function, contained more elongated mitochondria, showed reduced mitochondrial respiratory capacity, and showed a metabolic shift toward glycolysis for ATP production. Notably, Dnm1l^−/− NSCs exhibited impaired self-renewal ability and accelerated cellular aging during prolonged culture, resulting in decreased proliferation and cell death. Furthermore, Dnm1l^−/− NSCs showed elevated levels of inflammation and cell stress markers, suggesting a connection between Dnm1l deficiency and premature aging in NSCs. Therefore, the compromised self-renewal ability and accelerated cellular aging of Dnm1l^−/− NSCs may be attributed to mitochondrial fission defects.

As a novel cell type from eight-cell-stage embryos, extended pluripotent stem cells (EPSCs) are known for diverse differentiation potency in both extraembryonic and embryonic lineages, suggesting new possibilities as a developmental research model. Although various features of EPSCs have been defined, their ability to directly transfer extended pluripotency to differentiated somatic cells by cell fusion remains to be elucidated. Here, we derived EPSCs from eight-cell mouse embryos and confirmed their extended pluripotency at the molecular level and extraembryonic differentiation ability. Then, they were fused with OG2^+/− ROSA^+/− neural stem cells (NSCs) by the polyethylene-glycol (PEG)-mediated method and further analyzed. The resulting fused hybrid cells exhibited pluripotential markers with upregulated EPSC-specific gene expression. Furthermore, the hybrid cells contributed to the extraembryonic and embryonic lineages in vivo and in vitro. RNA sequencing analysis confirmed that the hybrid cells showed distinct global expression patterns resembling EPSCs without parental expression of NSC markers, indicating the complete acquisition of extended pluripotency and the erasure of the somatic memory of NSCs. Furthermore, ultrastructural observation and metabolic analysis confirmed that the hybrid cells rearranged the mitochondrial morphology and bivalent metabolic profile to those of EPSCs. In conclusion, the extended pluripotency of EPSCs could be transferred to somatic cells through fusion-induced reprogramming.

Retinal ganglion cell (RGC) degeneration is a hallmark of glaucoma and other optic neuropathies, yet the transcriptional mechanisms that drive stress-induced neuronal apoptosis remain incompletely understood. Here, we identify the developmental transcription factor PAX6 as an aberrantly sustained and stress-responsive regulator in mature retinal neurons. Upon NMDA-induced excitotoxic stress, PAX6 is phosphorylated by the neuronal stress kinase JNK3, without changes in total expression levels. In vitro kinase assays confirm direct phosphorylation of PAX6 by JNK3, while genetic ablation of JNK3 abolishes PAX6 activation. This phosphorylation enhances PAX6 chromatin binding and enables its co-recruitment with JNK3 to promoters of pro-apoptotic genes, including Bax and Gadd45a . Genome-wide ChIP-seq and transcriptomic analyses reveal that PAX6 and JNK3 form a transcriptional complex that drives apoptotic gene expression. In vivo, AAV-shRNA-mediated knockdown of either PAX6 or JNK3 significantly attenuates excitotoxic RGC death. These findings define a previously unrecognized transcriptional mechanism by which JNK3-mediated phosphorylation of persistently expressed PAX6 converts a developmental factor into a driver of neuronal apoptosis. More broadly, this study highlights how the dysregulation of developmental transcriptional programs in postmitotic neurons can contribute to neurodegeneration, offering new mechanistic insights into stress-induced neuronal loss in chronic neurodegenerative diseases.