Epigenetic states are crucial for cells to "remember" past events, such as environmental changes or developmental cues. These states are maintained by complex signals including transcription factors, noncoding RNAs, DNA methylation, and histone modifications. While these pathways regulate transcription, the mechanisms of epigenetic information transmission through cell division remain unclear. Epigenetic states are metastable and responsive to signals, making understanding their molecular basis essential for addressing disease-related epigenetic dysregulation. Epigenetic signals can be trans or cis. Trans signals are self-propagating and maintained through feedback loops, while cis signals are physically associated with DNA and inherited during cell division. Examples include DNA methylation and histone modifications. Trans signals can be maintained by self-sustaining transcriptional states, while cis signals are encoded in chromatin through modifications or associations with non-histone proteins. Epigenetic states are established by transient factors responding to environmental or developmental cues. Transcription factors (TFs) play a key role in this process, influencing cis epigenetic states. For example, in Drosophila, TFs establish cell fate during early development, and the Polycomb group (PcG) and trithorax group (trxG) proteins maintain these states. These proteins have chromatin-modifying activities, and in the absence of DNA methylation, the PcG/trxG system is likely involved in epigenetic state transmission. Epigenetic states can be reinforced locally or spread to adjacent areas. Feedback loops involving histone modifiers and binders help maintain these states. For example, SUV39H1 and HP1 for H3K9me, PR-SET7 and L3MBTL1 for H4K20me1, and EZH2 and EED for H3K27me are involved in this process. Spreading of chromatin domains is essential for epigenetic regulation, as seen in position-effect variegation in Drosophila and silent domains in yeast. Epigenetic states can also be reinforced by cross-talk between histone modifications and DNA methylation. For instance, de novo DNA methyltransferases bind to unmethylated H3K4, while the H3K4 methyltransferase MLL binds to unmethylated DNA, explaining the anti-correlation between H3K4me and DNA methylation. H3K9me is a prerequisite for DNA methylation in some organisms. DNA methylation satisfies all three criteria for epigenetic signals: propagation, transmission, and effect on gene expression. Histone modifications are less clear, but some show strong correlation with transcriptional states. Propagation mechanisms for histone modifications involve similar interactions as those for signal reinforcement and spreading. Epigenetic signals are transmitted through various mechanisms, including DNA methylation, histone modifications, and non-coding RNAs. These signals can be transmitted transgenerationally through meiosis andEpigenetic states are crucial for cells to "remember" past events, such as environmental changes or developmental cues. These states are maintained by complex signals including transcription factors, noncoding RNAs, DNA methylation, and histone modifications. While these pathways regulate transcription, the mechanisms of epigenetic information transmission through cell division remain unclear. Epigenetic states are metastable and responsive to signals, making understanding their molecular basis essential for addressing disease-related epigenetic dysregulation. Epigenetic signals can be trans or cis. Trans signals are self-propagating and maintained through feedback loops, while cis signals are physically associated with DNA and inherited during cell division. Examples include DNA methylation and histone modifications. Trans signals can be maintained by self-sustaining transcriptional states, while cis signals are encoded in chromatin through modifications or associations with non-histone proteins. Epigenetic states are established by transient factors responding to environmental or developmental cues. Transcription factors (TFs) play a key role in this process, influencing cis epigenetic states. For example, in Drosophila, TFs establish cell fate during early development, and the Polycomb group (PcG) and trithorax group (trxG) proteins maintain these states. These proteins have chromatin-modifying activities, and in the absence of DNA methylation, the PcG/trxG system is likely involved in epigenetic state transmission. Epigenetic states can be reinforced locally or spread to adjacent areas. Feedback loops involving histone modifiers and binders help maintain these states. For example, SUV39H1 and HP1 for H3K9me, PR-SET7 and L3MBTL1 for H4K20me1, and EZH2 and EED for H3K27me are involved in this process. Spreading of chromatin domains is essential for epigenetic regulation, as seen in position-effect variegation in Drosophila and silent domains in yeast. Epigenetic states can also be reinforced by cross-talk between histone modifications and DNA methylation. For instance, de novo DNA methyltransferases bind to unmethylated H3K4, while the H3K4 methyltransferase MLL binds to unmethylated DNA, explaining the anti-correlation between H3K4me and DNA methylation. H3K9me is a prerequisite for DNA methylation in some organisms. DNA methylation satisfies all three criteria for epigenetic signals: propagation, transmission, and effect on gene expression. Histone modifications are less clear, but some show strong correlation with transcriptional states. Propagation mechanisms for histone modifications involve similar interactions as those for signal reinforcement and spreading. Epigenetic signals are transmitted through various mechanisms, including DNA methylation, histone modifications, and non-coding RNAs. These signals can be transmitted transgenerationally through meiosis and