Meiotic recombination between homologous chromosomes is promoted by the collaborative action of two RecA homologs, Rad51 and meiosis-specific Dmc1. The filament assembly of Dmc1 is promoted by meiosis-specific Mei5–Sae3 in budding yeast. Mei5–Sae3 shows sequence similarity to fission yeast Sfr1–Swi5, which stimulates DNA strand exchanges by Rad51 as well as Dmc1. Sae3 and Swi5 share a conserved motif with the amino acid sequence YNEI/LK/RD. In this study, we analyzed the role of the YNEL residues in the Sae3 sequence in meiotic recombination and found that these residues are critical for Sae3 function in Dmc1 assembly. L59 substitution in the Sae3 protein disrupts complex formation with Mei5, while Y56 and N57 substitutions do not. These observations reveal the differential contribution of conserved YNEL residues to Sae3 activities in meiotic recombination.

Southeast Asia supports high biodiversity, in a mosaic of forest types formed by the expansion and contraction of habitats through past climate changes. Among the region's forest types, the geographical distribution of peat swamp forests has fluctuated intensely over the past 120,000 years. Most peat swamp forests in Southeast Asia are found in coastal regions and formed within the last 7,000 years after a decline in sea level. However, some peat swamps were initiated earlier on substrates of slightly higher elevation, and these peat swamps might have been refugia for peat swamp species in the last glacial period and the high sea level period. We assessed genetic diversity, genetic structure and divergence time of current genetic groups for Shorea albida in Brunei, an endemic tree species of Bornean peat swamp forests, using 18 microsatellite markers. Genetic diversity was not lower than has been found in other Shorea species, possibly because of the high density of S. albida in Brunei. Although overall genetic divergence between populations was low, two populations (Ingei and Labi Road 3) were distinct from the other populations. Analysis using DIYABC estimated that three genetic groups (Ingei, Labi Road 3 and others) diverged simultaneously from their ancestral population, whose effective size was very small, about 7,500 years ago, corresponding to a recent sea level peak in the Belait-Baram river basin. In that high sea level period, some higher-elevation lands remained, and peat formation had already started in this region. We propose that the current genetic structure of S. albida in Brunei was formed from small refugial populations that survived the period of higher sea level in these higher-elevation areas. Because of their relatively high genetic diversity, Brunei's S. albida populations should become an important genetic resource for the recovery of genetically healthy populations in other parts of northwest Borneo.

Posttranslational modifications (PTMs) to proteins are regulatory mechanisms that play a critical role in regulating growth and development. The SUMO system is a rapid and dynamic PTM system employed by eukaryotic cells. Plant SUMOs are involved in many physiological processes, such as stress responses, regulation of flowering time and defense reactions to pathogen attack. In Arabidopsis thaliana and rice (Oryza sativa), eight and seven SUMO genes, respectively, were predicted by sequence analysis. Phylogenetic tree analysis of these SUMOs shows that they are divided into two groups. One consists of SUMOs that contain no SUMO acceptor site and are involved in monoSUMOylation of their target proteins. Rice OsSUMO1 and OsSUMO2 are in this group, and are structurally similar to each other and to Arabidopsis AtSUMO1. The other group is composed of SUMOs in which an acceptor site (ΨKXE/D) occurs inside the SUMO molecule, suggesting their involvement in polySUMOylation. Several studies on the rice SUMOs have been performed independently and reported. Individual names of rice SUMOs are confusing, because a unified nomenclature has not been proposed. This review clarifies the attribution of seven rice SUMOs and unifies the individual SUMO names.

Plaque vulnerability is associated with the degree of carotid artery stenosis (CS) and the risk of stroke. MicroRNAs (miRNAs) exert critical functions in disease progression, although only a few miRNAs have been well identified in CS. Therefore, this study aimed to investigate the differential expression profile of miRNAs and their potential functions in plaques of CS patients. Three CS patients with stable plaques and three patients with vulnerable plaques who underwent carotid endarterectomy were enrolled in this study. Differentially expressed miRNAs (DEmiRNAs) between patients with stable and vulnerable plaques were determined using small RNA sequencing. Target genes of DEmiRNAs were predicted and submitted to functional analyses. Validation of dysregulated DEmiRNAs was determined using quantitative real-time polymerase chain reaction (qRT-PCR). After sequencing, 76 DEmiRNAs were identified in vulnerable plaques, including 53 upregulated miRNAs and 23 downregulated miRNAs. Next, 23,495 target genes of the identified DEmiRNAs were predicted and functionally analyzed. This indicated that the target genes of the identified DEmiRNAs were mainly enriched in protein phosphorylation, transcription, nitrogen compound metabolism, endocytosis and autophagy, and related to signaling pathways of Hippo, MAPK, insulin, TGF-β, FoxO, AMPK and p53. Furthermore, qRT-PCR results for six miRNAs showed that five (83%) of them (hsa-miR-511-5p, hsa-miR-150-5p, hsa-miR-378a-5p, hsa-miR-365b-5p and hsa-miR-6511b-5p) were consistent with the sequencing results. Differential expression profiles and potential function of miRNAs associated with plaque stability in CS patients are identified for the first time, which should help to understand the regulatory mechanism of plaque stability in CS.

Mechanisms underlying how the genetic code was generated by Darwinian selection have remained elusive since the code was cracked in 1965. Here, I propose a hypothesis on the emergence of the genetic code and predict that its emergence was driven by sequential distinct selective pressures. According to the hypothesis, aminoacyl-RNAs for Glu, Asp, Lys, Tyr, His, Arg, Cys and Ser were first selected as cartridge-type subunits of three-subunit ribozymes. Aminoacyl-RNA subunits acting as cofactors were accommodated by the proto P-site of the large subunit of ribozymes. Importantly, I predict that there was no direct relationship between amino acids and codon and anticodon pairs. Duplication of the proto P-site could have created the proto A-site, enabling multi-subunit ribozymes to simultaneously interact with two-cartridge-type aminoacyl-RNA subunits. Random insertion of two cartridges would have instantly abolished enzymatic activity of multi-subunit ribozymes. On the other hand, if two tandemly aligned pairs of codons and anticodons specify two cartridges, dozens of different active pockets in multi-subunit ribozymes would have rapidly emerged, leading to the rise of extant organisms' metabolic pathways. The strong driving force of Darwinian selection described here could have created the primary genetic code for catalytic amino acids. Evolution of the protein translation system and events leading to the expansion of the genetic code until the time it was "frozen" are presented in detail.

Genome sequencing revealed that nearly half of the human genome is comprised of transposable elements. Although most of these elements have been rendered inactive due to mutations, full-length intact long interspersed element-1 (LINE-1 or L1) copies retain the ability to mobilize through RNA intermediates by a so-called "copy-and-paste" mechanism, termed retrotransposition. L1 is the only known autonomous mobile genetic element in the genome, and its retrotransposition contributes to inter- or intra-individual genetic variation within the human population. However, L1 retrotransposition also poses a threat to genome integrity due to gene disruption and chromosomal instability. Moreover, recent studies suggest that aberrant L1 expression can impact human health by causing diseases such as cancer and chronic inflammation that might lead to autoimmune disorders. To counteract these adverse effects, the host cells have evolved multiple layers of defense mechanisms at the epigenetic, RNA and protein levels. Intriguingly, several host factors have also been reported to facilitate L1 retrotransposition, suggesting that there is competition between negative and positive regulation of L1 by host factors. Here, we summarize the known host proteins that regulate L1 activity at different stages of the replication cycle and discuss how these factors modulate disease-associated phenotypes caused by L1.

Organisms have evolved elaborate mechanisms that maintain genome stability. Deficiencies in these mechanisms result in changes to the nucleotide sequence as well as copy number and structural variations in the genome. Genome instability has been implicated in numerous human diseases. However, genomic alterations can also be beneficial as they are an essential part of the evolutionary process. Organisms sometimes program genomic changes that drive genetic and phenotypic diversity. Therefore, genome alterations can have both positive and negative impacts on cellular growth and functions, which underscores the need to control the processes that restrict or induce such changes to the genome. The ribosomal RNA gene (rDNA) is highly abundant in eukaryotic genomes, forming a cluster where numerous rDNA copies are tandemly arrayed. Budding yeast can alter the stability of its rDNA cluster by changing the rDNA copy number within the cluster or by producing extrachromosomal rDNA circles. Here, we review the mechanisms that regulate the stability of the budding yeast rDNA cluster during repair of DNA double-strand breaks that are formed in response to programmed DNA replication fork arrest.