Search bioRxiv⌕ Search

Biology subjects

Bartos, O.

Publications and source records attributed to Bartos, O..

2 recordsLinked to original sources

Revealing genomic changes responsible for cannabinoid receptor loss in parrots: mechanism and functional effects

In vertebrates, an ancient duplication in the genes for cannabinoid receptors (CNRs) allowed the evolution of specialised endocannabinoid receptors expressed in the brain (CNR1) and the periphery (CNR2). While dominantly conserved throughout vertebrate phylogeny, our comparative genomic analysis suggests that certain taxa may have lost either the CNR1 regulator of neural processes or, more frequently, the CNR2 involved in immune regulation. Focussing on conspicuous CNR2 pseudogenization in parrots (Psittaciformes), a diversified crown lineage of cognitively-advanced birds, we highlight possible functional effects of such a loss. Parrots appear to have lost the CNR2 gene at at least two separate occasions due to chromosomal rearrangement. Using gene expression data from the brain and periphery of birds with experimentally-induced sterile inflammation, we compare CNR and inflammatory marker (interleukin 1 beta, IL1B) expression patterns in CNR2-deficient parrots (represented by the budgerigar, Melopsittacus undulatus and five other parrot species) with CNR2-intact passerines (represented by the zebra finch, Taeniopygia guttata). Though no significant changes in CNR expression were observed in either parrots or passerines during inflammation of the brain or periphery, we detected a significant up-regulation of IL1B expression in the brain after stimulation with lipopolysaccharide (LPS) only in parrots. As our analysis failed to show evidence for selection on altered CNR1 functionality in parrots, compared to other birds, CNR1 is unlikely to be involved in compensation for CNR2 loss in modulation of the neuroimmune interaction. Thus, our results provide evidence for the functional importance of CNR2 pseudogenization for regulation of neuroinflammation.

genomics↗

Genome fractionation and loss of heterozygosity in hybrids and polyploids: mechanisms, consequences for selection and link to gene function

AbstractHybridization and genome duplication have played crucial roles in the evolution of many animal and plant taxa. During their evolution, the subgenomes of parental species undergo considerable changes in hybrids and polyploids, which often selectively eliminate segments of one subgenome. However, the mechanisms underlying these changes are not well understood, particularly when the hybridization is linked with asexual reproduction that may enforce specific evolutionary pathways. We studied the genome evolution in asexual diploid and polyploid hybrids between fish from the genus Cobitis. Comparing exome sequencing with published cytogenetic and RNAseq data revealed that clonal genomes remain static on chromosome-scale levels but undergo considerable small-scale restructurations owing to two major processes; hemizygous deletions and gene conversions. Interestingly, polyploids were much more tolerant to accumulating deletions than diploid asexuals where gene conversions prevailed. The genomic restructurations accumulated preferentially in genes characterized by high transcription levels, relatively strong purifying selection and some specific functions such as interacting with intracellular membranes. The likelihood of an orthologs retention or loss correlated with its parental-species ancestry, GC content, and expression. Furthermore, all hybrids showed a strong bias towards the retention of one parental subgenome. Contrary to expectations, however, the preferentially retained subgenome was not transcriptionally dominant as all hybrids were phenotypically more similar to the other parent. The present study demonstrated that the fate of subgenomes in asexual hybrids and polyploids depends on the complex interplay of selection and several molecular mechanisms whose impact depends on ploidy, sequence composition, gene expression as well as parental ancestry.

evolutionary biology↗