BSXplorer: analytical framework for exploratory analysis of BS-seq data.

BACKGROUND: Bisulfite sequencing detects and quantifies DNA methylation patterns, contributing to our understanding of gene expression regulation, genome stability maintenance, conservation of epigenetic mechanisms across divergent taxa, epigenetic inheritance and, eventually, phenotypic variation. Graphical representation of methylation data is crucial in exploring epigenetic regulation on a genome-wide scale in both plants and animals. This is especially relevant for non-model organisms with poorly annotated genomes and/or organisms where genome sequences are not yet assembled on chromosome level. Despite being a technology of choice to profile DNA methylation for many years now there are surprisingly few lightweight and robust standalone tools available for efficient graphical analysis of data in non-model systems. This significantly limits evolutionary studies and agrigenomics research. BSXplorer is a tool specifically developed to fill this gap and assist researchers in explorative data analysis and in visualising and interpreting bisulfite sequencing data more easily. RESULTS: BSXplorer provides in-depth graphical analysis of sequencing data encompassing (a) profiling of methylation levels in metagenes or in user-defined regions using line plots and heatmaps, generation of summary statistics charts, (b) enabling comparative analyses of methylation patterns across experimental samples, methylation contexts and species, and (c) identification of modules sharing similar methylation signatures at functional genomic elements. The tool processes methylation data quickly and offers API and CLI capabilities, along with the ability to create high-quality figures suitable for publication. CONCLUSIONS: BSXplorer facilitates efficient methylation data mining, contrasting and visualization, making it an easy-to-use package that is highly useful for epigenetic research.

Pygenomics: manipulating genomic intervals and data files in Python.

SUMMARY: We present pygenomics, a Python package for working with genomic intervals and bioinformatic data files. The package implements interval operations, provides both API and CLI, and supports reading and writing data in widely used bioinformatic formats, including BAM, BED, GFF3, and VCF. The source code of pygenomics is provided with in-source documentation and type annotations and adheres to the functional programming paradigm. These features facilitate seamless integration of pygenomics routines into scripts and pipelines. The package is implemented in pure Python using its standard library only and contains the property-based testing framework. Comparison of pygenomics with other Python bioinformatic packages with relation to features and performance is presented. The performance comparison covers operations with genomic intervals, read alignments, and genomic variants and demonstrates that pygenomics is suitable for computationally effective analysis. AVAILABILITY AND IMPLEMENTATION: The source code is available at https://gitlab.com/gtamazian/pygenomics.

Transcriptomic Analysis of Flowering Time Genes in Cultivated Chickpea and Wild Cicer.

Chickpea (Cicer arietinum L.) is a major grain legume and a good source of plant-based protein. However, comprehensive knowledge of flowering time control in Cicer is lacking. In this study, we acquire high-throughput transcriptome sequencing data and analyze changes in gene expression during floral transition in the early flowering cultivar ICCV 96029, later flowering C. arietinum accessions, and two wild species, C. reticulatum and C. echinospermum. We identify Cicer orthologs of A. thaliana flowering time genes and analyze differential expression of 278 genes between four species/accessions, three tissue types, and two conditions. Our results show that the differences in gene expression between ICCV 96029 and other cultivated chickpea accessions are vernalization-dependent. In addition, we highlight the role of FTa3, an ortholog of FLOWERING LOCUS T in Arabidopsis, in the vernalization response of cultivated chickpea. A common set of differentially expressed genes was found for all comparisons between wild species and cultivars. The direction of expression change for different copies of the FT-INTERACTING PROTEIN 1 gene was variable in different comparisons, which suggests complex mechanisms of FT protein transport. Our study makes a contribution to the understanding of flowering time control in Cicer, and can provide genetic strategies to further improve this important agronomic trait.

Genetic Determinants of Fiber-Associated Traits in Flax Identified by Omics Data Integration.

In this paper, we explore potential genetic factors in control of flax phenotypes associated with fiber by mining a collection of 306 flax accessions from the Federal Research Centre of the Bast Fiber Crops, Torzhok, Russia. In total, 11 traits were assessed in the course of 3 successive years. A genome-wide association study was performed for each phenotype independently using six different single-locus models implemented in the GAPIT3 R package. Moreover, we applied a multivariate linear mixed model implemented in the GEMMA package to account for trait correlations and potential pleiotropic effects of polymorphisms. The analyses revealed a number of genomic variants associated with different fiber traits, implying the complex and polygenic control. All stable variants demonstrate a statistically significant allelic effect across all 3 years of the experiment. We tested the validity of the predicted variants using gene expression data available for the flax fiber studies. The results shed new light on the processes and pathways associated with the complex fiber traits, while the pinpointed candidate genes may be further used for marker-assisted selection.

Genomic Regions Associated with Fusarium Wilt Resistance in Flax.

Modern flax cultivars are susceptible to many diseases; arguably, the most economically damaging of these is the Fusarium wilt fungal disease. Over the past decades international flax breeding initiatives resulted in the development of resistant cultivars. However, much remains to be learned about the mechanisms of resistance to Fusarium infection in flax. As a first step to uncover the genetic factors associated with resistance to Fusarium wilt disease, we performed a genome-wide association study (GWAS) using 297 accessions from the collection of the Federal Research Centre of the Bast Fiber Crops, Torzhok, Russia. These genotypes were infected with a highly pathogenic Fusarium oxysporum f.sp. lini MI39 strain; the wilt symptoms were documented in the course of three successive years. Six different single-locus models implemented in GAPIT3 R package were applied to a selected subset of 72,526 SNPs. A total of 15 QTNs (Quantitative Trait Nucleotides) were detected during at least two years of observation, while eight QTNs were found during all three years of the experiment. Of these, ten QTNs occupied a region of 640 Kb at the start of chromosome 1, while the remaining QTNs mapped to chromosomes 8, 11 and 13. All stable QTNs demonstrate a statistically significant allelic effect across 3 years of the experiment. Importantly, several QTNs spanned regions that harbored genes involved in the pathogen recognition and plant immunity response, including the KIP1-like protein (Lus10025717) and NBS-LRR protein (Lus10025852). Our results provide novel insights into the genetic architecture of flax resistance to Fusarium wilt and pinpoint potential candidate genes for further in-depth studies.

A Genomic Blueprint of Flax Fungal Parasite Fusarium oxysporum f. sp. lini.

Fusarium wilt of flax is an aggressive disease caused by the soil-borne fungal pathogen Fusarium oxysporum f. sp. lini. It is a challenging pathogen presenting a constant threat to flax production industry worldwide. Previously, we reported chromosome-level assemblies of 5 highly pathogenic F. oxysporum f. sp. lini strains. We sought to characterize the genomic architecture of the fungus and outline evolutionary mechanisms shaping the pathogen genome. Here, we reveal the complex multi-compartmentalized genome organization and uncover its diverse evolutionary dynamics, which boosts genetic diversity and facilitates host adaptation. In addition, our results suggest that host of functions implicated in the life cycle of mobile genetic elements are main contributors to dissimilarity between proteomes of different Fusaria. Finally, our experiments demonstrate that mobile genetics elements are expressed in planta upon infection, alluding to their role in pathogenicity. On the whole, these results pave the way for further in-depth studies of evolutionary forces shaping the host-pathogen interaction.

The Genome Sequence of Five Highly Pathogenic Isolates of Fusarium oxysporum f. sp. lini.

Fusarium wilt is the most destructive fungal disease in flax, limiting flax cultivation in all the main flax and linseed growing countries. The causative agent is seedborne and soilborne fungus F. oxysporum f. sp. lini. Here, we report, for the first time, genome assemblies of five highly pathogenic isolates of Fusarium oxysporum f. sp. lini, namely monoisolate 39 and strains F329, F324, F282, F287. In addition, syntenic analysis provided a powerful approach to distinguish between core and lineage-specific parts of the genome. These results lay a solid foundation for comparative genomics studies of plant fungal pathogens, evolution of pathogenicity, and virulence factors underlying the dynamics of host-pathogen interactions, thus eventually offering solutions to Fusarium disease control.

A point mutation in the ion conduction pore of AMPA receptor GRIA3 causes dramatically perturbed sleep patterns as well as intellectual disability.

The discovery of genetic variants influencing sleep patterns can shed light on the physiological processes underlying sleep. As part of a large clinical sequencing project, WGS500, we sequenced a family in which the two male children had severe developmental delay and a dramatically disturbed sleep-wake cycle, with very long wake and sleep durations, reaching up to 106-h awake and 48-h asleep. The most likely causal variant identified was a novel missense variant in the X-linked GRIA3 gene, which has been implicated in intellectual disability. GRIA3 encodes GluA3, a subunit of AMPA-type ionotropic glutamate receptors (AMPARs). The mutation (A653T) falls within the highly conserved transmembrane domain of the ion channel gate, immediately adjacent to the analogous residue in the Grid2 (glutamate receptor) gene, which is mutated in the mouse neurobehavioral mutant, Lurcher. In vitro, the GRIA3(A653T) mutation stabilizes the channel in a closed conformation, in contrast to Lurcher. We introduced the orthologous mutation into a mouse strain by CRISPR-Cas9 mutagenesis and found that hemizygous mutants displayed significant differences in the structure of their activity and sleep compared to wild-type littermates. Typically, mice are polyphasic, exhibiting multiple sleep bouts of sleep several minutes long within a 24-h period. The Gria3A653T mouse showed significantly fewer brief bouts of activity and sleep than the wild-types. Furthermore, Gria3A653T mice showed enhanced period lengthening under constant light compared to wild-type mice, suggesting an increased sensitivity to light. Our results suggest a role for GluA3 channel activity in the regulation of sleep behavior in both mice and humans.

Clinical whole-genome sequencing from routine formalin-fixed, paraffin-embedded specimens: pilot study for the 100,000 Genomes Project.

PURPOSE: Fresh-frozen (FF) tissue is the optimal source of DNA for whole-genome sequencing (WGS) of cancer patients. However, it is not always available, limiting the widespread application of WGS in clinical practice. We explored the viability of using formalin-fixed, paraffin-embedded (FFPE) tissues, available routinely for cancer patients, as a source of DNA for clinical WGS. METHODS: We conducted a prospective study using DNAs from matched FF, FFPE, and peripheral blood germ-line specimens collected from 52 cancer patients (156 samples) following routine diagnostic protocols. We compared somatic variants detected in FFPE and matching FF samples. RESULTS: We found the single-nucleotide variant agreement reached 71% across the genome and somatic copy-number alterations (CNAs) detection from FFPE samples was suboptimal (0.44 median correlation with FF) due to nonuniform coverage. CNA detection was improved significantly with lower reverse crosslinking temperature in FFPE DNA extraction (80 °C or 65 °C depending on the methods). Our final data showed somatic variant detection from FFPE for clinical decision making is possible. We detected 98% of clinically actionable variants (including 30/31 CNAs). CONCLUSION: We present the first prospective WGS study of cancer patients using FFPE specimens collected in a routine clinical environment proving WGS can be applied in the clinic.

Clinical whole-genome sequencing in severe early-onset epilepsy reveals new genes and improves molecular diagnosis.

In severe early-onset epilepsy, precise clinical and molecular genetic diagnosis is complex, as many metabolic and electro-physiological processes have been implicated in disease causation. The clinical phenotypes share many features such as complex seizure types and developmental delay. Molecular diagnosis has historically been confined to sequential testing of candidate genes known to be associated with specific sub-phenotypes, but the diagnostic yield of this approach can be low. We conducted whole-genome sequencing (WGS) on six patients with severe early-onset epilepsy who had previously been refractory to molecular diagnosis, and their parents. Four of these patients had a clinical diagnosis of Ohtahara Syndrome (OS) and two patients had severe non-syndromic early-onset epilepsy (NSEOE). In two OS cases, we found de novo non-synonymous mutations in the genes KCNQ2 and SCN2A. In a third OS case, WGS revealed paternal isodisomy for chromosome 9, leading to identification of the causal homozygous missense variant in KCNT1, which produced a substantial increase in potassium channel current. The fourth OS patient had a recessive mutation in PIGQ that led to exon skipping and defective glycophosphatidyl inositol biosynthesis. The two patients with NSEOE had likely pathogenic de novo mutations in CBL and CSNK1G1, respectively. Mutations in these genes were not found among 500 additional individuals with epilepsy. This work reveals two novel genes for OS, KCNT1 and PIGQ. It also uncovers unexpected genetic mechanisms and emphasizes the power of WGS as a clinical tool for making molecular diagnoses, particularly for highly heterogeneous disorders.

Recessive mutations in SPTBN2 implicate ß-III spectrin in both cognitive and motor development.

ß-III spectrin is present in the brain and is known to be important in the function of the cerebellum. Heterozygous mutations in SPTBN2, the gene encoding ß-III spectrin, cause Spinocerebellar Ataxia Type 5 (SCA5), an adult-onset, slowly progressive, autosomal-dominant pure cerebellar ataxia. SCA5 is sometimes known as "Lincoln ataxia," because the largest known family is descended from relatives of the United States President Abraham Lincoln. Using targeted capture and next-generation sequencing, we identified a homozygous stop codon in SPTBN2 in a consanguineous family in which childhood developmental ataxia co-segregates with cognitive impairment. The cognitive impairment could result from mutations in a second gene, but further analysis using whole-genome sequencing combined with SNP array analysis did not reveal any evidence of other mutations. We also examined a mouse knockout of ß-III spectrin in which ataxia and progressive degeneration of cerebellar Purkinje cells has been previously reported and found morphological abnormalities in neurons from prefrontal cortex and deficits in object recognition tasks, consistent with the human cognitive phenotype. These data provide the first evidence that ß-III spectrin plays an important role in cortical brain development and cognition, in addition to its function in the cerebellum; and we conclude that cognitive impairment is an integral part of this novel recessive ataxic syndrome, Spectrin-associated Autosomal Recessive Cerebellar Ataxia type 1 (SPARCA1). In addition, the identification of SPARCA1 and normal heterozygous carriers of the stop codon in SPTBN2 provides insights into the mechanism of molecular dominance in SCA5 and demonstrates that the cell-specific repertoire of spectrin subunits underlies a novel group of disorders, the neuronal spectrinopathies, which includes SCA5, SPARCA1, and a form of West syndrome.

Pangenomics of flax fungal parasite Fusarium oxysporum f. sp. lini.

To assess the genomic diversity of Fusarium oxysporum f. sp. lini strains and compile a comprehensive gene repertoire, we constructed a pangenome using 13 isolates from four different clonal lineages, each exhibiting distinct levels of virulence. Syntenic analyses of two selected genomes revealed significant chromosomal rearrangements unique to each genome. A comprehensive examination of both core and accessory pangenome content and diversity points at an open genome state. Additionally, Gene Ontology (GO) enrichment analysis indicated that non-core pangenome genes are associated with pathogen recognition and immune signaling. Furthermore, the Folini pansecterome, encompassing secreted proteins critical for fungal pathogenicity, primarily consists of three functional classes: effector proteins, CAZYmes, and proteases. These three classes account for approximately 3.5% of the pangenome. Each functional class within the pansecterome was meticulously annotated and characterized with respect to pangenome category distribution, PFAM domain frequency, and strain virulence assessment. This analysis revealed that highly virulent isolates have specific types of PFAM domains that are exclusive to them. Upon examining the repertoire of SIX genes known for virulence in other formae speciales, it was found that all isolates had a similar gene content except for two, which lacked SIX genes entirely.

A collection of read depth profiles at structural variant breakpoints.

SWaveform, a newly created open genome-wide resource for read depth signal in the vicinity of structural variant (SV) breakpoints, aims to boost development of computational tools and algorithms for discovery of genomic rearrangement events from sequencing data. SVs are a dominant force shaping genomes and substantially contributing to genetic diversity. Still, there are challenges in reliable and efficient genotyping of SVs from whole genome sequencing data, thus delaying translation into clinical applications and wasting valuable resources. SWaveform includes a database containing ~7 M of read depth profiles at SV breakpoints extracted from 911 sequencing samples generated by the Human Genome Diversity Project, generalised patterns of the signal at breakpoints, an interface for navigation and download, as well as a toolbox for local deployment with user's data. The dataset can be of immense value to bioinformatics and engineering communities as it empowers smooth application of intelligent signal processing and machine learning techniques for discovery of genomic rearrangement events and thus opens the floodgates for development of innovative algorithms and software.

Host Genetic Variants Linked to COVID-19 Neurological Complications and Susceptibility in Young Adults-A Preliminary Analysis.

To date, multiple efforts have been made to use genome-wide association studies (GWAS) to untangle the genetic basis for SARS-CoV-2 infection susceptibility and severe COVID-19. However, data on the genetic-related effects of SARS-CoV-2 infection on the presence of accompanying and long-term post-COVID-19 neurological symptoms in younger individuals remain absent. We aimed to examine the possible association between SNPs found in a GWAS of COVID-19 outcomes and three phenotypes: SARS-CoV-2 infection, neurological complications during disease progression, and long-term neurological complications in young adults with a mild-to-moderate disease course. University students (N = 336, age 18-25 years, European ancestry) with or without COVID-19 and neurological symptoms in anamnesis comprised the study sample. Logistic regression was performed with COVID-19-related phenotypes as outcomes, and the top 25 SNPs from GWAS meta-analyses and an MR study linking COVID-19 and cognitive deficits were found. We replicated previously reported associations of the FURIN and SLC6A20 gene variants (OR = 2.36, 95% CI 1.31-4.24) and OR = 1.94, 95% CI 1.08-3.49, respectively) and remaining neurological complications (OR = 2.12, 95% CI 1.10-4.35 for SLC6A20), while NR1H2 (OR = 2.99, 95% CI 1.39-6.69) and TMPRSS2 (OR = 2.03, 95% CI 1.19-3.50) SNPs were associated with neurological symptoms accompanying COVID-19. Our findings indicate that genetic variants related to a severe COVID-19 course in adults may contribute to the occurrence of neurological repercussions in individuals at a young age.

A Combined Effect of Polygenic Scores and Environmental Factors on Individual Differences in Depression Level.

The risk of depression could be evaluated through its multifactorial nature using the polygenic score (PGS) approach. Assuming a "clinical continuum" hypothesis of mental diseases, a preliminary assessment of individuals with elevated risk for developing depression in a non-clinical group is of high relevance. In turn, epidemiological studies suggest including social/lifestyle factors together with PGS to address the "missing heritability" problem. We designed regression models, which included PGS using 27 SNPs and social/lifestyle factors to explain individual differences in depression levels in high-education students from the Volga-Ural region (VUR) of Eurasia. Since issues related to population stratification in PGS scores may lead to imprecise variant effect estimates, we aimed to examine a sensitivity of PGS calculated on summary statistics of depression and neuroticism GWAS from Western Europeans to assess individual proneness to depression levels in the examined sample of Eastern Europeans. A depression score was assessed using the revised version of the Beck Depression Inventory (BDI) in 1065 young adults (age 18-25 years, 79% women, Eastern European ancestry). The models based on weighted PGS demonstrated higher sensitivity to evaluate depression level in the full dataset, explaining up to 2.4% of the variance (p = 3.42 × 10-7); the addition of social parameters enhanced the strength of the model (adjusted r2 = 15%, p < 2.2 × 10-16). A higher effect was observed in models based on weighted PGS in the women group, explaining up to 3.9% (p = 6.03 × 10-9) of variance in depression level assuming a combined SNPs effect and 17% (p < 2.2 × 10-16)-with the addition of social factors in the model. We failed to estimate BDI-measured depression based on summary statistics from Western Europeans GWAS of clinical depression. Although regression models based on PGS from neuroticism (depression-related trait) GWAS in Europeans were associated with a depression level in our sample (adjusted r2 = 0.43%, p = 0.019-for unweighted model), the effect was mainly attributed to the inclusion of social/lifestyle factors as predictors in these models (adjusted r2 = 15%, p < 2.2 × 10-16-for unweighted model). In conclusion, constructed PGS models contribute to a proportion of interindividual variability in BDI-measured depression in high-education students, especially women, from the VUR of Eurasia. External factors, including the specificity of rearing in childhood, used as predictors, improve the predictive ability of these models. Implementation of ethnicity-specific effect estimates in such modeling is important for individual risk assessment.

Long non-coding RNA-derived peptides are immunogenic and drive a potent anti-tumour response.

Protein arginine methyltransferase (PRMT) 5 is over-expressed in a variety of cancers and the master transcription regulator E2F1 is an important methylation target. We have explored the role of PRMT5 and E2F1 in regulating the non-coding genome and report here a striking effect on long non-coding (lnc) RNA gene expression. Moreover, many MHC class I protein-associated peptides were derived from small open reading frames in the lncRNA genes. Pharmacological inhibition of PRMT5 or adjusting E2F1 levels qualitatively altered the repertoire of lncRNA-derived peptide antigens displayed by tumour cells. When presented to the immune system as either ex vivo-loaded dendritic cells or expressed from a viral vector, lncRNA-derived peptides drove a potent antigen-specific CD8 T lymphocyte response, which translated into a significant delay in tumour growth. Thus, lncRNA genes encode immunogenic peptides that can be deployed as a cancer vaccine.

An account of Fusarium wilt resistance in flax Linum usitatissimum: The disease severity data.

A collection of flax accessions maintained by the Russian Federal Research Center for Bast Fiber Crops was characterized to evaluate its resistance to Fusarium wilt. 297 samples representing different morphotypes and selection status were infected with highly virulent MI39 strain of Fusarium oxysporum f. sp. lini. Evaluation of disease symptoms was performed at the full emergence stage in a greenhouse. The experiment lasted for 3 successive years. The disease severity index (DSI) record was obtained for every genotype in each year of the experiment. The data set was produced in a framework of a project focused on both a) deciphering the mechanisms of plant immunity, and b) development of flax cultivars resistant to Fusarium wilt. The data is available via Figshare repository.

A Genome-Wide Association Study Reveals a BDNF-Centered Molecular Network Associated with Alcohol Dependence and Related Clinical Measures.

At least 50% of factors predisposing to alcohol dependence (AD) are genetic and women affected with this disorder present with more psychiatric comorbidities, probably indicating different genetic factors involved. We aimed to run a genome-wide association study (GWAS) followed by a bioinformatic functional annotation of associated genomic regions in patients with AD and eight related clinical measures. A genome-wide significant association of rs220677 with AD (p-value = 1.33 × 10-8 calculated with the Yates-corrected χ2 test under the assumption of dominant inheritance) was discovered in female patients. Associations of AD and related clinical measures with seven other single nucleotide polymorphisms listed in previous GWASs of psychiatric and addiction traits were differently replicated in male and female patients. The bioinformatic analysis showed that regulatory elements in the eight associated linkage disequilibrium blocks define the expression of 80 protein-coding genes. Nearly 68% of these and of 120 previously published coding genes associated with alcohol phenotypes directly interact in a single network, where BDNF is the most significant hub gene. This study indicates that several genes behind the pathogenesis of AD are different in male and female patients, but implicated molecular mechanisms are functionally connected. The study also reveals a central role of BDNF in the pathogenesis of AD.

A comprehensive dataset of flax (Linum uitatissimum L.) phenotypes.

A collection of flax accessions from Russian Federal Research Center for Bast Fiber Crops was characterised to evaluate its phenotypic diversity. 406 samples representing different morphotypes were selected for thorough quantitative assessment of various agronomic traits. We measured height, length of technical part of the stem, technical part weight, inflorescence length, number of bolls and seeds per plant, 1000 seed weight, the diameter of the stem, the number of internodes and finally, distance between internodes. The fiber quality was estimated by calculating stem slenderness, stem taperingness and elementary fiber length. The dataset was produced in a framework of a project focused on characterization of diversity of flax genotypes and phenotypes, as well as on identification of genomic regions associated with various traits, it is hosted on Figshare.

Stochastic Effects in Retrotransposon Dynamics Revealed by Modeling under Competition for Cellular Resources.

Transposons are genomic elements that can relocate within a host genome using a 'cut'- or 'copy-and-paste' mechanism. They make up a significant part of many genomes, serve as a driving force for genome evolution, and are linked with Mendelian diseases and cancers. Interactions between two specific retrotransposon types, autonomous (e.g., LINE1/L1) and nonautonomous (e.g., Alu), may lead to fluctuations in the number of these transposons in the genome over multiple cell generations. We developed and examined a simple model of retrotransposon dynamics under conditions where transposon replication machinery competed for cellular resources: namely, free ribosomes and available energy (i.e., ATP molecules). Such competition is likely to occur in stress conditions that a malfunctioning cell may experience as a result of a malignant transformation. The modeling revealed that the number of actively replicating LINE1 and Alu elements in a cell decreases with the increasing competition for resources; however, stochastic effects interfere with this simple trend. We stochastically simulated the transposon dynamics in a cell population and showed that the population splits into pools with drastically different transposon behaviors. The early extinction of active Alu elements resulted in a larger number of LINE1 copies occurring in the first pool, as there was no competition between the two types of transposons in this pool. In the other pool, the competition process remained and the number of L1 copies was kept small. As the level of available resources reached a critical value, both types of dynamics demonstrated an increase in noise levels, and both the period and the amplitude of predator-prey oscillations rose in one of the cell pools. We hypothesized that the presented dynamical effects associated with the impact of the competition for cellular resources inflicted on the dynamics of retrotransposable elements could be used as a characteristic feature to assess a cell state, or to control the transposon activity.