Proposed model of the effect of Lamin B1 and B2 degradation on chromatin organization. Loss of B-type lamins induces nuclear blebbing and stalled cell cycle progression, indicating their structural and functional importance as components of the nuclear periphery. Although mid-range chromatin folding (e.g., TAD # and size, A/B compartmentalization, and contact probabilities in and outside LADs) is preserved, loss of these proteins promotes increased chromatin mobility along with an inward shift of chromosome territories (e.g., Chr. 1 and 2), heterochromatin-associated domains (e.g., LADs), and gene loci (red and yellow circles), especially at the nuclear periphery. The resulting genome-wide transcriptional changes both within and outside of LADs may be a direct consequence of heterochromatin redistribution and/or gene repositioning in relation to LADs upon the loss of structural constraints at the nuclear periphery
