Abstract
Development is a stepwise process in which multi-potent progenitor
cells undergo lineage commitment, differentiation, proliferation
and maturation to produce mature cells with restricted developmental
potentials. This process is directed by spatiotemporally distinct
gene expression programs that allow cells to stringently orchestrate
intricate transcriptional activation or silencing events. In eukaryotes,
chromatin structure contributes to developmental progression as a
blueprint for coordinated gene expression by actively participating
in the regulation of gene expression. Changes in higher order chromatin
structure or covalent modification of its components are considered
to be critical events in dictating lineage-specific gene expression
during development. Mammalian cells utilize multi-subunit nuclear
complexes to alter chromatin structure. Histone-modifying complex
catalyzes covalent modifications of histone tails including acetylation,
methylation, phosphorylation and ubiquitination. ATP-dependent chromatin
remodeling complex, which disrupts histone-DNA contacts and induces
nucleosome mobilization, requires energy from ATP hydrolysis for
its catalytic activity. Here, we discuss the diverse functions of
ATP-dependent chromatin remodeling complexes during mammalian development.
In particular, the roles of these complexes during embryonic and
hematopoietic development are reviewed in depth. In addition, pathological
conditions such as tumor development that are induced by mutation
of several key subunits of the chromatin remodeling complex are discussed,
together with possible mechanisms that underlie tumor suppression
by the complex.
- animals
- chromatin_assembly_and_disassembly
- chromosomal_proteins,_non-histone,_physiology
- dna_helicases,_physiology
- embryonic_development,_genetics
- genes,_switch,_physiology
- gene_expression_regulation
- growth_and_development,_genetics
- hematopoiesis,_genetics
- humans
- mice
- neoplasms,_genetics
- nuclear_proteins,_physiology
- t-lymphocytes,_physiology
- transcription_factors,_physiology
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