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Miklik, D.

Publications and source records attributed to Miklik, D..

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↗

Long Terminal Repeats of Gammaretroviruses Retain Stable Expression After Integration Retargeting or Knock-In into the Restrictive Chromatin of Lamina-Associated Domains

Retroviruses integrate their genomes into the genomes of infected host cells and form a genetic platform for stable gene expression. Epigenetic silencing can, however, hamper the expression of integrated provirus. As gammaretroviruses ({gamma}RVs) preferentially integrate into sites of active promoters and enhancers, the high expression activity of {gamma}RVs can be attributed to the integration preference. Long terminal repeats (LTRs) of some {gamma}RVs were shown to act as potent promoters for gene expression. Here, we investigate the capacity of different {gamma}RV LTRs to drive stable expression inside a non-preferred epigenomic environment using diverse retroviral vectors and CRISPR-Cas9-directed vector knock-in. We demonstrate that different {gamma}RV LTRs are either rapidly silenced or long-term active with active proviral population prevailing under normal and retargeted integration. In addition, we show that lamina-associated domains (LADs) can be targeted by CRISPR-Cas9 for vector insertion leading to {gamma}RV LTR-driven long-term stable gene expression. Alternatively to established {gamma}RV systems, the LTRs of feline leukemia virus and koala retrovirus are capable of driving stable, albeit intensity-diverse, transgene expression in LADs. Altogether, we show that despite the occurrence of rapid silencing events, the majority of {gamma}RV LTRs can drive stable expression after retrovirus integration or CRISPR-Cas9-directed knock-in outside of the preferred chromatin landscape.

molecular biology↗

Unraveling the Palindromic and Non-Palindromic Motifsof Retroviral Integration Site Sequences by Statistical Mixture Models

A weak palindromic nucleotide motif is the hallmark of retroviral integration site alignments. Previously, the motifs were explained by an overlap of the non-palindromic motif being present on one of the half-site of targeted sequences. Here, we applied multicomponent mixture models to integration site sequences of diverse retroviruses. We demonstrate that the weak palindromic motifs result from a combination of independent sub-motifs restricted to only a few positions proximal to the site of integration. The sub-motifs are formed by either palindrome-forming nucleotide preference or nucleotide exclusion. Using the mixture models, we also identified HIV-1-favored palindromic sequences in Alu repeats serving as hotspots for integration. Our work presents a novel statistical approach to the analysis of retroviral integration site sequences, which can form a valuable tool in the analysis of DNA motifs. The presented results shed new light on the selection of target site sequences for retroviral integration.

microbiology↗