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Figure: schematic diagram illustrating the different stages of embryonic development in mice, with the arrow indicating the time of implantation. Embryos lacking Zc3h11a are unable to survive after implantation, leading to degeneration.

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With over twenty thousand genes in the human body, the physiological functions of many genes remain elusive. A previous study by the same Swedish team had identified ZC3H11A as a pro-viral protein, as it is required for the efficient growth of several human viruses replicating in the nucleus, such as HIV. The ZC3H11A protein thus emerged as a promising therapeutic target for the development of antiviral agents. In the current study, the two teams have discovered an additional function of ZC3H11A at a precise moment of early embryonic growth in mice. ZC3H11A plays a central role in regulating the expression of metabolic genes crucial to the metabolic changes that occur in embryos around the time of implantation. Disruption or absence of ZC3H11A results in complete lethality of mouse embryos, and inactivation of this gene is likely to be lethal in other mammals, including humans. This groundbreaking discovery underscores the indispensable role of ZC3H11A in orchestrating the metabolic processes essential to embryo survival and development. The researchers then set out to study the impact of ZC3H11A deletion in adult organs. To do so, they developed an inducible mouse model that enabled them to eliminate ZC3H11A specifically after birth. The results of this study were surprising: complete inactivation of ZC3H11A in mouse tissues had no significant effects on cell growth or viability. The fact that depletion of ZC3H11A in adult tissues had no significant clinical consequences suggests that antiviral therapy based on ZC3H11A inactivation may not have significant side effects.