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Pajer, P.

Publications and source records attributed to Pajer, P..

3 recordsLinked to original sources

Decoding the avian missing gene mystery: dot chromosomes unmask extensive gene loss and novel genetic instability

The apparent absence of numerous conserved vertebrate genes from avian genomes has puzzled researchers for over a decade. In recent years, a subset of these genes has been identified; however, their sequences are unusually problematic, often evading detection by standard sequencing technologies. This limitation has hindered detailed investigation of the phenomenon--until recent progress in long read technologies, which are more robust against sequencing biases. This enabled us to classify real gene losses extensively, which strikingly revealed that a large number of the genes residing on so-called dot chromosomes were indeed lost during avian evolution. We demonstrate that dot microchromosomes--small, repeat-dense avian chromosomes--harbor widespread gene attrition, with 29% of ohnologs (duplicates from ancestral genome doublings) eliminated, far exceeding rates on other chromosomes. Moreover, we reveal that genes retained on these dot chromosomes exhibit a previously undescribed form of dynamic genetic instability. This instability, which we term sequence stuttering, is characterized by a massive expansion of short sequences within intronic regions. Intriguingly, in some cases, the expanding sequences appear to originate from neighboring exons. As a result, intron lengths vary extensively among individual chickens, suggesting that these events are evolutionarily recent. Since this phenomenon has not been reported in any other vertebrate species, our findings lay the groundwork for future research into its underlying mechanisms, evolutionary implications, and potential identification of similar loci across vertebrate genomes. SIGNIFICANCEThis study reveals extensive gene loss and a novel genetic instability, termed "sequence stuttering," on avian dot microchromosomes, providing new insights into avian genomic evolution. Approximately 29% of ohnologs on dot chromosomes are absent compared to other vertebrate chromosomes, possibly due to elevated GC content and recombination rates in euchromatin regions. This significant gene loss highlights dot chromosomes as hotspots for genomic reduction, potentially shaping avian-specific traits. Additionally, sequence stuttering--characterized by extensive intronic repeat expansions, sometimes incorporating exonic sequences--introduces marked length polymorphism within chicken populations, suggesting ongoing evolutionary dynamics. These findings underscore the unique role of dot chromosomes in avian genome evolution, emphasizing their contribution to genetic diversity and adaptation. This work lays the foundation for further investigation into the molecular mechanisms driving these phenomena and their broader implications for vertebrate genomic evolution.

genomics↗

Sex Chromosome Turnover and Structural Interspecific Genome Divergence Shapes Meiotic Outcomes in Hybridizing Cobitis

It has been empirically established that genome mixing between divergent species can trigger meiotic aberrations, ultimately leading to the emergence of asexual reproduction through the production of unreduced gametes in various metazoan lineages. Yet, it remains poorly understood how such asexual hybrids cope with co-inherited differences in sex determination systems, diverged regulatory networks, and chromosomal incompatibilities-- especially in the context of increased ploidy. Addressing these questions requires high-quality, chromosome-level reference genomes of the parental species involved in hybrid formation. Here, we present the first chromosome-level genome assemblies for three hybridizing Cobitis species (C. elongatoides, C. taenia, and C. tanaitica), providing a comprehensive framework to investigate the genetic and cytogenetic basis of hybrid sterility and the transition to asexuality. By integrating genome scaffolding, male/female pooled sequencing, and molecular cytogenetics, we uncover extensive structural variation among homologous chromosomes of the three species, despite their overall syntenic conservation. Population-level Pool-Seq analyses further revealed that each species possesses a distinct, non-homologous sex chromosome, highlighting sex chromosome turnover even among recently diverged lineages. These assemblies enabled the design of chromosome-specific painting probes, which we applied to meiotic metaphase I spreads of diploid hybrids. This approach revealed striking differences in the pairing success of orthologous chromosomes, with some (e.g., Ch01B) frequently forming bivalents, while others (e.g., Ch01A, Ch05, Ch20) failed to do so and remained unpaired. Our results demonstrate that chromosome-specific features, shaped by structural evolution and sex-linked divergence, contribute unequally to hybrid meiotic failure. Together, this work provides a high-resolution genomic and cytogenetic framework to understand how interspecific hybridization gives rise to clonality, and how the architecture of inherited parental genomes shapes the success or breakdown of meiosis in hybrid vertebrates.

genomics↗

Avian interferon regulatory factor (IRF) family reunion: IRF3 and IRF9 found

Interferon regulatory factors (IRFs) are a family of transcription factors in jawed vertebrates with important functions in immunity and many other key cellular processes. The genomes of most vertebrates encode ten IRF genes (IRF1 to IRF10). IRF3 and IRF9 have key roles in the interferon (IFN) induction and signaling. Most of our knowledge about the IFN pathways originates from the study of the mammalian IFN system, and the description of the corresponding avian components is not as complete. Both IRF3 and IRF9 were considered missing from the chicken genome and also from the genomes of all other avian species. Here we describe multiple avian IRF3 and IRF9 genes, all with difficult GC-rich sequence context which prevented their earlier characterization. IRF3 orthologs are more narrowly distributed and are present in the avian infraclass Palaeognathae residing in a syntenic genomic locus shared with other vertebrates. In contrast, IRF9 orthologs were found in most avian species with the notable exception of the order Galliformes. In about half of the avian orders analyzed, IRF9 was located in noncanonical chromosomal positions indicating past evolutionary translocations. Importantly, phylogenetic analysis confirmed the correct orthology of all newly described avian IRFs. We performed a series of experiments using duck (Anas platyrhynchos) IRF9, confirming its key role in the IFN signaling pathway. Knockout of IRF9 in duck embryonal fibroblasts decreases the induction of IFN-stimulated genes (ISGs). Full induction of ISGs in duck cells requires both intact IRF9 and canonical IFN-stimulated response element (ISRE). Lastly, intact IRF9 is needed for IFN-mediated protection of duck cells against vesicular stomatitis virus (VSV)-induced cytopathic effect. The identification of avian IRFs fills an important gap in our understanding of avian immunology and brings new questions related to the evolution of the IRF family.

immunology↗