Biology subjects

Novotna, P.

Publications and source records attributed to Novotna, P..

3 recordsLinked to original sources

bioRxiv2026

Cytogenomic signatures of hybridisation in the genus Carpobrotus reveal biased parental dominance

O_LIHybridisation is frequently associated with plant invasions; however, its consequences for genome organisation and chromosome evolution remain poorly understood in invasive species. We investigated the extent of hybridisation in the invasive Carpobrotus edulis--acinaciformis hybrid complex and determined the cytogenomic contribution of parental species in hybrid accessions. C_LIO_LIWe combined whole-genome sequencing, population genomic analyses, genome size estimation, repeatome characterisation, chromosome counting and fluorescence in situ hybridisation to compare parental species and hybrid accessions from South Africa and the Mediterranean Basin. C_LIO_LIPopulation genomic analyses revealed widespread hybridisation and introgression, with most invasive accessions showing admixed ancestries. Pattersons D-statistic supported asymmetric allele sharing towards C. edulis. Hybrid accessions displayed genome sizes indistinguishable from C. edulis, whereas C. acinaciformis possessed significantly larger genomes. Repeatome analyses identified marked differences in repetitive DNA composition, particularly in satellite DNA abundance and chromosomal distribution. A newly identified satellite repeat (CarpoSat) showed contrasting chromosomal patterns between parental species, whereas hybrids resembled C. edulis satellite pattern. C_LIO_LIOur results demonstrate that Carpobrotus hybrid accessions are a swarm of later-generation hybrids and backcrosses showing a strong bias towards C. edulis, indicating asymmetric introgression. These findings highlight the value of integrating cytogenetic and genomic approaches to understand genome evolution in invasive hybrid complexes. C_LI

plant biology↗

bioRxiv2025

Sex chromosome pairing and multivalent associations during meiosis in diploid and polyploid Silene latifolia

Sex chromosomes undergo various modifications that affect their synapsis during meiosis. While most of the genome achieves full synapsis by the end of pachytene, the non-recombining regions of XY (or ZW) chromosomes often remain asynaptic, and fail to form physical associations at metaphase I. Despite significant progress in animal models, the meiotic behaviour dynamics of plant sex chromosomes remain largely unexplored. In this study, we employed super-resolution microscopy to analyse 3D chromosome organization and the localization of key meiotic proteins. Namely, we studied the dynamics of ASY1, ZYP1, and HEI10, across the leptotene to pachytene stages, and compared sex chromosome behaviour in dioecious Silene latifolia with related gynodioecious S. vulgaris. Our findings show that both exhibits a class I crossover (CO) frequency comparable to mammals, indicating moderate COs per bivalent and their similar genetic determinants. We document variation in sex chromosome configurations, from rod bivalents in diploids to open-ring tetravalents in autopolyploids, and characterize Y chromosome behaviour across XXY, XXXY, and XXYY karyotypes. These results reveal pronounced variation in pairing and synaptic patterns, even within a shared genetic background. We discuss how these patterns reflect the evolutionary trajectory of the non-recombining region and provide the most detailed cytogenetic analysis of sex chromosome pairing in a plant with evolutionary young sex chromosomes.

cell biology↗

bioRxiv2024

Plectin-mediated cytoskeletal crosstalk as a target for inhibition of hepatocellular carcinoma growth and metastasis.

The most common primary malignancy of the liver, hepatocellular carcinoma (HCC), is a heterogeneous tumor entity with high metastatic potential and complex pathophysiology. Increasing evidence suggests that tissue mechanics plays a critical role in tumor onset and progression. Here we show that plectin, a major cytoskeletal crosslinker protein, plays a crucial role in mechanical homeostasis and mechanosensitive oncogenic signaling that drives hepatocarcinogenesis. Our expression analyses revealed elevated plectin levels in liver tumors, which correlated with poor prognosis for HCC patients. Using autochthonous and orthotopic mouse models we demonstrated that genetic and pharmacological inactivation of plectin potently suppressed the initiation and growth of HCC. Moreover, plectin targeting potently inhibited the invasion potential of human HCC cells and reduced their metastatic outgrowth in the lung. Proteomic and phosphoproteomic profiling linked plectin-dependent disruption of cytoskeletal networks to attenuation of oncogenic FAK, MAPK/Erk, and PI3K/AKT signatures. Importantly, by combining cell line-based and murine HCC models, we show that plectin inhibitor plecstatin-1 (PST) is well-tolerated and potently inhibits HCC progression. In conclusion, our study demonstrates that plectin-controlled cytoarchitecture is a key determinant of HCC development and suggests that pharmacologically induced disruption of mechanical homeostasis may represent a new therapeutic strategy for HCC treatment.

cancer biology↗