The steroidogenic acute regulatory protein (StAR) governs the rate-limiting step of steroid hormone biosynthesis by facilitating cholesterol transfer from the outer mitochondrial membrane (OMM) to the inner mitochondrial membrane (IMM). This essential function initiates pregnenolone synthesis by P450 family 11 subfamily A member 1 (CYP11A1, cytochrome P450scc) within IMM. Beyond its biochemical role, StAR is a critical developmental protein, with spatiotemporally restricted expression during fetal adrenal and gonadal differentiation. Its activity is tightly regulated at multiple levels, including transcriptional control by transcription factors, GATA post-translational phosphorylation, mitochondrial targeting, and proteolytic degradation. Structurally, StAR functions through a dynamic molten globule-like conformation and a conserved StAR-related lipid transfer (START) domain that mediates cholesterol binding. StAR interacts with mitochondrial proteins such as nonselective voltage-gated ion channel VDAC (VDAC), translocator protein (TSPO), and ATPase family AAA domaincontaining protein 3A (ATAD3A), forming part of the transduceosome complex that coordinates cholesterol transfer. Mutations in STAR, particularly within the START domain), cause lipoid congenital adrenal hyperplasia (CAH), a disorder marked by impaired steroidogenesis and disrupted endocrine organ development. This review integrates current knowledge on the molecular and developmental roles of STAR, emphasizing how its precise regulation is essential for embryonic steroidogenesis. Understanding StAR's function at the interface of lipid transport and organogenesis provides critical insight into congenital steroidogenic disorders and potential avenues for therapeutic intervention.

Oxybenzone (Benzophenone-3; BP-3) is used as a component of sunscreens, and known to disrupt the endocrine system of marine organisms. This study evaluated BP-3 toxicity on Shimofuri goby (Tridentiger bifasciatus). We evaluated morphological changes during embryogenesis. In addition, hatching rate (HR) and embryo survival to hatching were assessed. Embryos were exposed to BP-3 in artificial seawater, and then they were randomly sampled every 12 hours for microscopic observation and cortisol analysis. 36 hours after exposure to BP-3 100 and 1,000 ㎍/L groups, the tail was not separated from the yolk sac. 72 hours after exposure, incompleted eye pigmentation was observed at 100 and 1,000 ㎍/L BP-3. After 48 and 60 hours of exposure, all individuals in the control group had elongated tails, whereas individuals in the all BP-3 treated group failed to elongate or showed signs of bent tails. Survival rate decreased dose-dependently (control: >90%) with LC₅₀-96h=493 ㎍/L. HR significantly declined in all BP-3 groups in a dose-dependent manner. And, heartbeat was increased in response to BP-3 1,000 ㎍/L. High levels of cortisol were observed in the initial groups (0 hours) and decreased after 24 hours. The BP-3 100 and 1,000 ㎍/L showed significantly lower cortisol levels than the control at 96 hours of exposure. Overall, this study suggests that BP-3 can interfere with embryonic development, resulting in adverse effects on survival and HRs in T. bifasciatus embryos.

Neural progenitors of the ventral spinal cord differentiate into GABAergic Kolmer-Agduhr neurons (KA) under the control of Jagged2-meditated Notch signaling during late neurogenesis. Mib-mediated Notch signaling has also been demonstrated to regulate the number of KA neurons in the p3 domain. However, the relationship between Jagged2 and Mib during late neurogenesis remains unclear. Here we investigate how Mib is involved in the regulation of Jagged2 and the long-range Notch signaling. Ubiquitination of Jagged2 by Mib was found to promote its proteasome-dependent degradation in undifferentiated P19 cells, but not in differentiated P19 cells by retinoic acid. Co-IP assay revealed that Mib physically interacts with Jagged2, but not with the intracellular domain itself. Cell transplantation experiments showed that the formation of extracellular vesicles (EVs) containing Jagged2 was promoted by the co-expression of Mib. Our observations suggest that EVs containing Jagged2 and Mib may play a role in the Notch signaling in discrete compartments of the neural tube during the development of the vertebrate nervous system.