Ggps1, or geranylgeranyl diphosphate synthase 1, is a member of the prenyltransferase family. It functions in the mevalonate/isoprenoid pathway, catalyzing the synthesis of geranylgeranyl pyrophosphate, a lipid precursor for geranylgeranylated proteins like small guanosine triphosphatases [2]. This process is crucial as abnormal Ggps1 expression can disrupt protein farnesylation and geranylgeranylation balance, affecting various cellular physiological and pathological processes [3].

In a myometrial cell-specific Ggps1-deleted mouse model, Ggps1 deficiency in the uterus led to impaired uterine contractions, disrupted embryonic placing, and dystocia. Mechanistically, Ggps1 is required for uterine contractions by regulating RhoA prenylation to activate the RhoA/Rock2/p-MLC pathway [1]. Also, a Ggps1 Y259C knock-in mouse resulted in prenatal lethality, indicating the importance of Ggps1 in normal development [2].

In conclusion, Ggps1 is essential for processes such as uterine contraction during parturition and normal development. Its deficiency can lead to severe consequences like dystocia and prenatal lethality. Research on Ggps1 using mouse models has provided insights into its role in these biological processes and diseases related to muscular dystrophy, hearing loss, and ovarian insufficiency [1,2].