Portal de Periódicos da CAPES

Dealing with Gene-Dosage Imbalance during S Phase

2016; Elsevier BV; Volume: 32; Issue: 11 Linguagem: Inglês

10.1016/j.tig.2016.08.006

1362-4555

Raz Bar‐Ziv, Yoav Voichek, Naama Barkai,

Bacterial Genetics and Biotechnology

Gene dosage becomes transiently imbalanced during DNA replication. In bacteria, expression increases immediately following replication, introducing growth rate-dependent biases that are capitalized for regulation. In eukaryotes, the effect of changes in gene dosage during DNA replication on expression is buffered. In budding yeast, buffering gene expression during DNA replication is chromatin based and is dependent on acetylation of H3K56 by Rtt109/Asf1. DNA replication perturbs the dosage balance between genes that replicate early during S phase and those that replicate late. If propagated to influence protein content, this dosage imbalance could influence cellular functions. In bacteria, mechanisms have evolved to use this imbalance to tune certain processes with the rate of cell growth. By contrast, eukaryotes buffer this dosage imbalance to ensure gene expression homeostasis also during S phase. Here, we outline classical and more recent studies describing how different organisms deal with this replication-dependent dosage imbalance, and describe recent results linking the eukaryotic buffering mechanism to replication-dependent histone acetylation. Finally, we discuss the possible implications of this buffering mechanism and speculate why it is specific to eukaryote cells. DNA replication perturbs the dosage balance between genes that replicate early during S phase and those that replicate late. If propagated to influence protein content, this dosage imbalance could influence cellular functions. In bacteria, mechanisms have evolved to use this imbalance to tune certain processes with the rate of cell growth. By contrast, eukaryotes buffer this dosage imbalance to ensure gene expression homeostasis also during S phase. Here, we outline classical and more recent studies describing how different organisms deal with this replication-dependent dosage imbalance, and describe recent results linking the eukaryotic buffering mechanism to replication-dependent histone acetylation. Finally, we discuss the possible implications of this buffering mechanism and speculate why it is specific to eukaryote cells.