LIN54 is an essential core subunit of the DREAM/LINC (LIN complex) and MuvB complexes. These complexes play crucial roles in the coordinated regulation of cell cycle genes, either activating transcription during S-G2 phases or repressing it during quiescence [1,3,4]. LIN54 is required for cell cycle progression and has a DNA-binding domain (CHC domain) which consists of two cysteine-rich (CXC) domains, enabling it to bind to the cdc2 promoter in a sequence-specific manner [1].

In Drosophila, the LIN54 homolog Mip120 controls two aspects of oogenesis. Its absence leads to egg chamber arrest during the transition from stage 7 to 8 due to failure in normal chromosomal dynamics in ovarian nurse cells, and also causes a dramatic increase in the expression of benign gonial cell neoplasm (bgcn) [2]. In mouse embryonic stem cells (ESCs), deficiency of Lin54 triggers G2/M arrest, loss of pluripotency, and spontaneous differentiation, and these abnormalities can be partially rescued by ectopic co-expression of Cyclin B1 and Cdk1 [5].

In conclusion, LIN54 is vital for cell cycle regulation and has a significant impact on processes such as oogenesis and maintaining embryonic stem cell identity. The study of LIN54 through model-based research, like in Drosophila and mouse ESCs, provides insights into its role in normal development and potentially in disease conditions related to cell cycle dysregulation [2,5].