Chuanshuai Xie

The ancestor of all vertebrates is thought to have undergone autopolyploid whole-genome duplication (WGD) ^1,2 , doubling the genetic raw material for evolutionary diversification ^3–5 . However, we still do not understand the first steps of rediploidization that followed, required for the emergence and divergence of duplicated genes (ohnologues) created by WGD ^6,7 . Consequently, how the functional potential created by autopolyploidy becomes realized during evolution remains unclear. Snow carps (Schizothoracine) have a history of recent WGDs and evolved high-altitude adaptations ^8–10 , making these fish a particularly suitable system to study the early stages and consequences of rediploidization. Here genomic data from all snow carp genera reveal their autopolyploid origin, including tetraploids, hexaploids and one icosaploid (20 n ). We present haplotype-resolved genomes for two snow carp species ( Schizopygopsis younghusbandi and Schizothorax curvilabiatus ) from divergent lineages, revealing a single ancestral autotetraploidy event. Comparative genomic, meiotic pairing and allele composition analyses indicate that unbalanced chromosome fusions were responsible for the transition from tetrasomic to disomic inheritance, creating genomic regions harbouring diploid ohnologue pairs, with non-rearranged chromosomes remaining tetraploid. This study suggests that this mechanism initiated rediploidization and documents its early chromosomal and genomic consequences. It starts at chromosome fusion sites and expands outwards towards chromosomal arms, a process that remained incomplete post-speciation, leading to a mixture of ancestral and lineage-specific ohnologue divergence on highly syntenic chromosomes.

Hypsibarbus vernayi (2n = 50), a medium-sized barb distributed in the Mekong River basin, is widely consumed in its native range and holds significant potential for commercial aquaculture development. To date, there is no high-quality genome available for this species. In this study, we generated a haplotype-resolved and near-T2T assembly of H. vernayi utilizing PacBio HiFi, Oxford Nanopore and Hi-C technologies. The assembled genome sizes for two haplotypes are 709 Mb and 707 Mb with scaffold N50 of 27.8 Mb and 26.8 Mb, respectively. A 262-bp satellite DNA sequence was identified as the centromeric repeats that appeared on almost all chromosomes. The diploid genome contains only eight gaps: one and seven in the two haploid genomes, respectively. Furthermore, 31 out of 50 chromosomes have telomeres assembled at both ends. This high-quality reference genome is expected to facilitate the breeding efforts for this species.

Root-knot nematodes (RKNs) of the genus Meloidogyne pose the most significant threats to global food security due to their destructive nature as plant-parasitic nematodes. Although significant attention has been devoted to investigating the gene transcription profiling of RKNs, our understanding of the translational landscape of RKNs remains limited. In this study, we elucidated the translational landscape of Meloidogyne incognita through the integration of translatome, transcriptome and quantitative proteome analyses. Our findings revealed numerous previously unannotated translation events and refined the genome annotation. By investigating the genome-wide translational dynamics of M. incognita during parasitism, we revealed that the genes of M. incognita undergo parasitic stage-specific regulation at the translational level. Interestingly, we identified 470 micropeptides (containing fewer than 100 amino acids) with the potential to function as effectors. Additionally, we observed that the effector-coding genes in M. incognita exhibit higher translation efficiency (TE). Further analysis suggests that M. incognita has the potential to regulate the TE of effector-coding genes without simultaneous alterations in their transcript abundance, facilitating effector synthesis. Collectively, our study provides comprehensive datasets and explores the genome-wide translational landscape of M. incognita, shedding light on the contributions of translational regulation during parasitism.

KDM5C influence H3K4me3 peaks width via its histone demethylase activity.

Delineating KDM5C and BRD4 localization and illustrating the definitions of transcriptional elements.

Loss of KDM5C sensitize tumor cells to BETi treatment.

BRD4 is a vulnerability of KDM5C deficient tumor cells.

PROTAC drugs compound 3b degrades KDM5C in multiples cell lines and promotes BRD4 chromatin dissociation.

PROTAC drugs compound 3b degrades KDM5C in multiples cell lines and promotes BRD4 chromatin dissociation.

BRD4 is a vulnerability of KDM5C deficient tumor cells.