Abstract
The number and complexity of genes encoding nuclear lamina proteins has increased during metazoan evolution. Emerging evidence reveals that transcriptional repressors such as the retinoblastoma protein, and apoptotic regulators such as CED-4, have functional and dynamic interactions with the lamina. The discovery that mutations in nuclear lamina proteins cause heritable tissue-specific diseases, including Emery–Dreifuss muscular dystrophy, is prompting a fresh look at the nuclear lamina to devise models that can account for its diverse functions and dynamics, and to understand its enigmatic structure.
Keywords
nuclear lamina; apoptosis; transcription; retroblastoma protein
The main feature of eukaryotic cells is the nucleus, which enwraps the chromosomes and is the site of DNA replication, RNA transcription and processing, and ribosome assembly. The nuclear envelope (NE) is the boundary between the nucleus and cytoplasm. The NE is composed of the inner and outer nuclear membranes (INM and ONM, respectively), which are separated by a lumenal space continuous with the ER lumen. Communication between the nucleoplasm and cytoplasm takes place through pores in the nuclear envelope, where the inner and outer membranes join. Within these pores are nuclear pore complexes (NPCs), which mediate and regulate nuclear transport 1. Underneath the INM is a meshwork of nuclear-specific intermediate filaments, termed the nuclear lamina, which includes lamin proteins plus a growing number of lamin-associated proteins 2. and 3.. Near the INM is the peripheral chromatin, a large proportion of which is heterochromatin (Fig. 1).