Relatively semi-conservative replication and a folded slippage model for simple sequence repeats

Abstract

Simple sequence repeats (SSRs) are found ubiquitously in almost all genome, and their formation mechanism is ambiguous yet. Here, the SSRs were analyzed in 55 randomly selected segments of genomes from a fairly wide range of species, with introducing more open standard for extensively mining repeats. A high percentage of repeats were discovered in these segments through that open standard and verified that they are not random. However, the current theory suggested that repeats tend to disappear over long-term evolution, which is inconsistent with such high proportion of SSRs remained in the genomes, inferring that there is most probably a mechanism for continually producing repeats during replicating process to balance continuous repeat disappearance. It can be inferred that there is most probably a mechanism for continually producing repeats during replicating process to balance continuous repeats disappearance, which certainly makes the base numbers of replication strand unequal to template strand. Therefore, the accepted straight-line slippage model is necessary to improve for explaining occurrence of simple sequence repeats. We proposed a folded slippage model to explain the high percent microsatellite occurrence with considering the geometric space of nucleotides and hydrogen bond stability, which can describe microsatellite expansion and contraction more reasonably. And analysis of external forces in the folding template strands showed the microsatellites tend to expand than contract. Our research may provide implements for the contribution of microsatellites to genome evolution and complement the semi-conservative replication.

Cell wall-resident PIR proteins show an inverted architecture inNeurospora crassa, but keep their role as wall stabilizers

“…The variable number of PIR domains might be the result of an equal number of intragenic PIR domain duplications, which usually occur in the middle of the protein, and mechanistically might be explained by DNA replication slippage [93][94][95][96][97]. Tandem repeat expansion is a mechanism of rapid protein evolution with phenotypic consequences (cell surface variability for fast adaptation to diverse environments) observed in fungi [8,27,98,99], but also in other kingdoms [100].…”