Project description:ARID1A, a subunit of the switch/sucrose non-fermentable (SWI/SNF) chromatin remodeling complex, influences gene accessibility. However, the role of ARID1A in spatial genomic organization and chromosomal interaction remains elusive. We showed that the SWI/SNF complex interacts with condensin II and they show significant overlapping distributions in enhancers. ARID1A inactivation drives redistribution of condensin II preferentially at enhancers without affecting the interaction between the SWI/SNF and condensing II complexes. ARID1A and condensin II contribute to transcriptionally inactive B compartments, while ARID1A weakens the borders of topologically associated domains. ARID1A inactivation decreases the frequency of genomic interactions over distance, but increases the intermixing of interphase small chromosomes, which was validated by three dimensional chromosome painting. These results demonstrated ARID1A spatially partitions genome and chromosomes.
Project description:ARID1A, a subunit of the switch/sucrose non-fermentable (SWI/SNF) chromatin remodeling complex, influences gene accessibility. However, the role of ARID1A in spatial genomic organization and chromosomal interaction remains elusive. We showed that the SWI/SNF complex interacts with condensin II and they show significant overlapping distributions in enhancers. ARID1A inactivation drives redistribution of condensin II preferentially at enhancers without affecting the interaction between the SWI/SNF and condensing II complexes. ARID1A and condensin II contribute to transcriptionally inactive B compartments, while ARID1A weakens the borders of topologically associated domains. ARID1A inactivation decreases the frequency of genomic interactions over distance, but increases the intermixing of interphase small chromosomes, which was validated by three dimensional chromosome painting. These results demonstrated ARID1A spatially partitions genome and chromosomes.
Project description:ARID1A, a subunit of the switch/sucrose non-fermentable (SWI/SNF) chromatin remodeling complex, influences gene accessibility. However, the role of ARID1A in spatial genomic organization and chromosomal interaction remains elusive. We showed that the SWI/SNF complex interacts with condensin II and they show significant overlapping distributions in enhancers. ARID1A inactivation drives redistribution of condensin II preferentially at enhancers without affecting the interaction between the SWI/SNF and condensing II complexes. ARID1A and condensin II contribute to transcriptionally inactive B compartments, while ARID1A weakens the borders of topologically associated domains. ARID1A inactivation decreases the frequency of genomic interactions over distance, but increases the intermixing of interphase small chromosomes, which was validated by three dimensional chromosome painting. These results demonstrated ARID1A spatially partitions genome and chromosomes.
Project description:Condensins are multi-subunit protein complexes that regulate chromosome structure throughout cell-cycle. Metazoans contain two types of condensin complexes (I and II) with essential and distinct functions. In C. elegans a third type of condensin (IDC) functions as part of the X chromosome dosage compensation complex1,2. We mapped genome-wide binding sites of the three condensin types in C. elegans embryos. Characteristics of condensin binding are similar between condensin types. ChIP-seq profiles of C. elegans subunits of the three condensins in 3-6 replicates from mixed stage embryos, controls are included, and RNA-Seq profiles of C. elegans in 5 replicates from mixed staged embryos. Additionally, ChIP-seq profiles of the condensin II subunit KLE-2 in 6 replicates from L3 with controls, and RNA-Seq profiles of KLE-2 mutants in 3 replicates each from L3.
Project description:Condensins are multi-subunit protein complexes that regulate chromosome structure throughout cell-cycle. Metazoans contain two types of condensin complexes (I and II) with essential and distinct functions. In C. elegans a third type of condensin (IDC) functions as part of the X chromosome dosage compensation complex1,2. We mapped genome-wide binding sites of the three condensin types in C. elegans embryos. Characteristics of condensin binding are similar between condensin types.
Project description:During mitosis, condensin activity is thought to disrupt interphase chromatin structures. Here, we utilize condensin-deficient mitotic chromosomes as a unique architectural platform to further investigate genome folding principles. Upon condensin loss, compartments progressively emerge in mitotic chromosomes. Euchromatin diverges into two different compartments A1 and A2, the former of which shows strong homotypic interactions while the latter exhibit reduced self-aggregation. Constitutive heterochromatin (B1) displays reduced level of compartmentalization and the normally inert facultative heterochromatin (B2) participates to compartmentalize the genome. Dynamically, A1 compartment is established remarkably fast with similarly efficient separation from B1 while reformation of B1 is delayed, implying that A1 self-attraction is the engine to compartmentalizalize the condensin-depleted mitotic chromosomes. Notified by the mitotic compartmentalization of B1 which lacks HP1 binding, we sought to explore the role of HP1 proteins in genome folding and demonstrat that HP1& are dispensible for chromatin structural restoration during cell divison. Our observations unveil delicate patterns and novel principles of genome compartmentalization that are otherwise hidden in interphase cells.