Gene conversion: a non-Mendelian process integral to meiotic recombination

Abstract

Meiosis is undoubtedly the mechanism that underpins Mendelian genetics. Meiosis is a specialised, reductional cell division which generates haploid gametes (reproductive cells) carrying a single chromosome complement from diploid progenitor cells harbouring two chromosome sets. Through this process, the hereditary material is shuffled and distributed into haploid gametes such that upon fertilisation, when two haploid gametes fuse, diploidy is restored in the zygote. During meiosis the transient physical connection of two homologous chromosomes (one originally inherited from each parent) each consisting of two sister chromatids and their subsequent segregation into four meiotic products (gametes), is what enables genetic marker assortment forming the core of Mendelian laws. The initiating events of meiotic recombination are DNA double-strand breaks (DSBs) which need to be repaired in a certain way to enable the homologous chromosomes to find each other. This is achieved by DSB ends searching for homologous repair templates and invading them. Ultimately, the repair of meiotic DSBs by homologous recombination physically connects homologous chromosomes through crossovers. These physical connections provided by crossovers enable faithful chromosome segregation. That being said, the DSB repair mechanism integral to meiotic recombination also produces genetic transmission distortions which manifest as postmeiotic segregation events and gene conversions. These processes are non-reciprocal genetic exchanges and thus non-Mendelian.

The Transcriptome and Proteome Networks of Malignant Tumours Reveal Atavistic Attractors of Polyploidy-Related Asexual Reproduction

“…On the other side, between those who do not doubt the programmatic atavistic development of cancer, there is a controversy over the time of its evolutionary origin, unicellular or early multicellular [ 60 , 61 , 62 ]. More fundamentally, there is also no clarity on the functional role of the meiotic toolkit in polyploidy-including life-cycles of the obligatory agamic protists [ 63 , 64 ]. In this study, we approach these questions by means of complex network analysis on publicly available cancer patient datasets (transcriptomes, inferred ploidy/WGD values, phylostratigraphy, and proteomes).…”

Microarray and in silico analysis of DNA repair genes between human testis of patients with nonobstructive azoospermia and normal cells

“…40,41 Hundreds of DNA double-strand breaks are produced and repaired during meiotic recombination, enabling genetic information to be transferred across homologous chromosomes. 42 The failure to repair DNA damage adequately is known to cause a halt in the development of germ cells and sterility inside the animal. 43 The BRG1 component of the SWI/SNF complex, in particular, has been found to be essential for the effective completion of meiosis.…”

Repeat-induced point mutation and gene conversion coinciding with heterochromatin shape the genome of a plant pathogenic fungus

“…Gene conversion is initiated by DSBs, followed by resection of the DSB end and the invasion of the single-stranded tail into homologous sequences. Sequence differences between the two homologous sequences will result in partially mismatched heteroduplex DNA (5,25,29). If the mismatch is repaired using the information of the invading DNA the acceptor allele will be changed to the donor allele and hence result in gene conversion as manifested by a 3:1 rather than 2:2 segregation pattern in the resulting products of a single meiosis -a tetrad.…”

“…If the mismatch is repaired using the information of the invading DNA the acceptor allele will be changed to the donor allele and hence result in gene conversion as manifested by a 3:1 rather than 2:2 segregation pattern in the resulting products of a single meiosis – a tetrad. Heteroduplex DNA and repair also occur during crossover (CO) events and hence gene conversions can be categorized into those associated with CO (CO-GC) and those associated with non-crossover NCO (NCO-GC) (29). Rates of gene conversion vary considerably between species (30, 31) which appears to be mainly influenced by the tract length (i.e.…”