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Post-polyploid chromosomal diploidization in plants is affected by clade divergence and constrained by shared genomic features
Abstract Genomic redundancy following whole-genome duplication creates opportunities for double-strand misrepair that can lead to chromosomal rearrangements and reductions in chromosome number, known as descending dysploidy. Although flowering plants often undergo post-polyploid rediploidization, the pathways and consequences of descending dysploidy remain poorly understood. Here, we sequence and assemble the genomes of eight Biscutella species ranging from 0.6 to 1.1 Gb and exhibiting chromosome numbers of n = 6, 8 and 9. Our analysis reveals ~11 million years of diploidization from an allotetraploid ancestor with n = 14, characterized by independent descending dysploidy. We identify early-diverging ( n = 8/6) and late-diverging ( n = 9) genomes that share convergent and divergent features. While both clades show similar levels of gene fractionation and preferential retention of polyploidy-derived genes, the early-diverging genomes exhibit a higher solo-to-intact ratio of Ty3/Gypsy long terminal repeat retrotransposons and fewer conserved topologically associated domains (TADs). We also identify 14 chromosome breakpoints frequently located at TAD boundaries and often associated with transitions between A and B compartments. These results suggest that, although post-polyploid descending dysploidy appears to be independent and superficially stochastic, shared genomic features may predispose recurrent chromosome breakpoints across species.
Structural basis for a filamentous morpheein model of human cystathionine beta-synthase
Abstract Human cystathionine beta-synthase (CBS) is a vital enzyme that regulates sulfur amino acid metabolism, hydrogen sulfide production, and cellular redox balance. Using a multidisciplinary approach, we demonstrate that CBS functions as a filamentous morpheein, with its stability, turnover, and activity governed by dynamic quaternary structural transitions. Three distinct filamentous assemblies were resolved by cryo-EM and are mediated by the oligomerization loop (residues 516–525): (i) ligand-free trans -dimers that form trans -basal filaments with basal stability and activity, (ii) adenosylornithine-bound cis -dimers that assemble into stabilized cis -basal filaments and (iii) S-adenosylmethionine-bound allo -dimers, which, together with cis -dimers, form highly stable, allo -activated stacked filaments. These reversible filamentous assemblies redefine CBS biology by integrating oligomerization and allosteric regulation within a morpheein framework. These findings provide a transformative perspective on CBS function and open avenues for pharmacological targeting of dysregulated CBS in various diseases including homocystinuria, cancer, and Down syndrome.
Human angiotensin‑converting enzyme 2‑specific benzothiazole-based allosteric inhibitor against pan‑sarbecoviruses
Ultrafast Photothermal Conversion of Ru/Zn Heterometallic Metal–Organic Framework for Synergistic Catalytic CO <sub>2</sub> Fixation
Optimized PI based fuzzy controller for power quality assessment in autonomous microgrid using novel hybrid bio-inspired optimization technique
Yield estimation and operational parameter evaluation of three crude oils using aspen HYSYS simulation-based
Explainable ensemble learning for estimating strength and stiffness of clay-bearing rocks: A case study from the Gurpi formation, Iran
Relationships between body composition, lipid metabolism, and platelet fatty acid profiles in women with anorexia nervosa: a cross-sectional study
Clinical investigation of a digital biomarker for joint swelling in inflammatory arthritis based on automated quantification of dorsal finger fold patterns
Low KIF4A expression is associated with gastric cancer progression and aggressive phenotypes
An adaptive emotion aware music education system using machine learning for personalized emotional wellbeing enhancement
An effective BiLSTM-CNN model for predicting large-scale temporal-spatial dynamics of normalized difference vegetation index
Algorithm selection for lithium-ion battery ECM parameterization: a comparative study of trust-region, Levenberg-Marquardt, Gauss-Newton, and BFGS for accuracy and physical consistency
Robust displacement estimation from filament-based soft sensors using a parallel attention-enhanced LSTM for rehabilitation monitoring
The normative measures for Chinese Reading Acuity Test (CRAT) in Cantonese-speaking children
Interferon-gamma release assay screening before solid organ transplantation in a low-incidence country: a prospective single-center cohort study
Induced chromosomal instability in triple negative breast cancer cells promotes M2-like polarization of macrophages
Abstract Chromosomal instability (CIN) is a defining feature of triple-negative breast cancer (TNBC) and is increasingly recognized as a driver of tumor evolution and immune escape. However, how CIN HIGH tumor cells modulate innate immune cells, particularly macrophages, remains unclear. Here, we used the MPS1 inhibitor reversine to induce acute CIN in the TNBC cell line MDA-MB-231 and examined its impact on human macrophage polarization and function. Reversine-induced CIN stably increased the expression of macrophage-attracting cytokines, including CCL2, CCL5, and IL-6. In direct co-cultures, reversine-treated cancer cells promoted M2-like macrophage polarization, accompanied by a modest increase of M1-like markers, whereas in non-contact transwell co-cultures, soluble paracrine signals from reversine-treated TNBC cells only promoted M2-like polarization. Furthermore, macrophages exposed to reversine-treated TNBC cells showed enhanced uptake of cancer cells, further underscoring their activation by cells with reversine-induced CIN. Finally, we found that macrophage activation coincided with the secretion of factors that promoted cancer cell migration, suggesting that immune-cancer cell interaction promotes metastasis. Together, our findings show that drug-induced CIN in TNBC cells promotes polarization of co-cultured macrophages, promoting an immunosuppressive, pro-migratory niche that may be exploitable for therapies targeting CIN-associated immune modulation.