bioRxiv Science⌕ Search

Biology subjects

Pulido Barrera, D. C.

Publications and source records attributed to Pulido Barrera, D. C..

2 recordsLinked to original sources

Safeguarding epithelial junctions by a novel quality control pathway

Cell junctions establish and maintain epithelial architecture despite fluctuating environmental and developmental conditions. A central question is how cells respond to challenging conditions to preserve junctional integrity. Here, we report the discovery of a previously unrecognized quality control pathway that monitors epithelial junctions (J-QC). We used the (I)Caenorhabditis elegans(/I) epidermis as a model to investigate the DLG-1-AJM-1 complex (DAC), a junctional domain that is critical for embryonic morphogenesis. We identify two mechanisms that sustain junctional integrity: first, localized (I)dlg-1(/I) mRNA ensures appropriate DLG-1 protein levels at the junction; repositioning (I)dlg-1(/I) RNA reduces DLG-1 levels, leading to gaps between epithelial cells. Second, transcription of DAC components responds to perturbations that disrupt the DAC. This response is sequence-independent, distinguishing it from other quality control mechanisms. It is activated by perturbations of the DAC or cytoskeleton and requires the LINC complex component ZYG-12/HOOK1-3 to transduce information about junctional integrity to the nucleus. These findings define a novel junctional QC for epithelial maintenance.

cell biology↗

Single-molecule chromosome tracing reveals a diversity of megabase heterochromatin domains

Chromosomes fold into distinct domains that regulate transcription, replication, and repair. Beyond well-characterized TADs and compartments, the diversity of heterochromatin domains remains poorly defined at the sequence level. Using single-molecule tracing of nascent heterochromatin in C. elegans, we identify three classes of megabase-scale domains: (i) sharp-boundary, Condensin I-dependent Topological Associating Domain-like domains (TADLs); (ii) similarly sized, but Condensin-independent, elegans Condensin-Independent Domains (elCIDs); and (iii) weaker, diffuse structures that are abundant in the population. TADLs arise early in development, preceding elCIDs, and both become progressively compacted through H3K9 methylation, which promotes intra- and inter-domain proximity. Condensin mutations disrupt TADLs, yet single molecules can still form domain-like structures, as recapitulated by free polymer simulations. However, these differ markedly in boundary positioning and biophysical properties. Our results uncover previously unrecognized heterochromatin architectures and demonstrate that single-molecule analysis and mutational dissection provide valuable approaches for distinguishing between domain types.

genomics↗