We clarified the phylogeny and population structure of foxtail millet (Setaria italica (L.) P.Beauv.) landraces using ddRAD-seq, which also enabled us to focus in detail on Japanese landraces. The results were compared with those of previous phylogenetic studies based on transposon display and genotyping of individual genes involved in domestication and diversification under natural and artificial selection. Foxtail millet landraces were found to cluster into distinct geographical groups. The comparison revealed that certain genes, such as Heading date 1 (HD1) and polyphenol oxidase (Si7PPO), began diverging soon after domestication. In contrast, genes such as Pseudo-response regulator 37 (SiPRR37) appeared to have differentiated before geographic divergence, likely in response to environmental adaptation. However, genes such as Waxy (Wx) loci diversified after geographic separation under human selection. Implication of introgression between geographically distant groups was also observed, for example, between French and East Asian landraces. In Japan, two distinct landrace groups were identified: one closely related to Korean landraces and the other showing genetic similarity to accessions from Taiwan and the Batan Islands of the Philippines. The latter group is predominantly distributed in the Nansei Islands (Okinawa Prefecture), indicating multiple introductions and complex dispersal histories of foxtail millet in Japan.

Japanagromyza tokunagai Sasakawa 1953 (Agromyzidae, Diptera) disrupts seed reproduction of orchids by feeding on orchid fruit. This species has been feeding on orchid fruits in Japan for more than 100 years, but the recent increase in damage may be due to the spread of particularly harmful populations. In this study, we used nanopore sequencing to establish microsatellite markers for J. tokunagai to infer the cause of this fly's spreading history based on population genetic analysis of historical specimen origin and current samples. Analysis of three populations showed that all 15 loci of microsatellite markers established were polymorphic and the number of alleles ranged between 3 and 13. The markers developed in this study can be used to reveal current and past population genetic diversity and gene flow, contributing to our understanding of the population history of this parasitic fly. Further research using these markers will provide a foundation for the developing control methods for J. tokunagai and support the conservation of rare orchid plants.

Cold acclimation, defined as gradual habituation to low temperatures by exposure to mild cold temperatures for several days, has been known to enhance an organism's cold tolerance and facilitate its adaptation to seasonal temperature changes in temperate regions. The present study focuses on the evolution of the cold acclimation response in Drosophila albomicans, which rapidly expanded its distribution from tropical Southeast Asia to Japanese main islands in the mid-1980s. This research aims to elucidate the genetic mechanisms underlying cold acclimation through gene expression changes. The gene expression changes due to cold acclimation were compared among five strains with different genetic backgrounds to identify the genes involved in these processes. High-throughput mRNA sequencing (RNA-seq) was employed to identify differentially expressed genes (DEGs) in strains from China, Taiwan, and Japan under cold acclimation and control conditions. The results suggest that the actin genes play a critical role in cellular functions at low temperatures. A reduction in the expression of mElo is likely to result in decreased levels of C18 fatty acids, thereby enhancing cellular cold tolerance. Furthermore, this study highlights the universality and diversity of gene expression changes in response to cold acclimation. While many DEGs shared by all five strains were the genes involved in metabolic pathways, many strain-specific DEGs were the genes involved in gene regulation. This suggests that the genes with critical roles in fundamental cellular and physiological processes are subject to evolutionary constraints, and that the genes involved in regulatory functions or responding to local environmental conditions may undergo rapid evolution to exhibit significant variability. These results provide insight into the genetic mechanisms of environmental adaptation and population expansion in nature.

VANDAL family DNA transposons are prevalent in Arabidopsis and related plants. A notable feature of VANDALs is that they can overcome epigenetic silencing from the host, using a VANC protein encoded in each VANDAL member: VANC21 protein encoded in VANDAL21 specifically accumulates on its target DNA motifs that are concentrated in the non-coding regions of this TE and induces loss of DNA methylation, transcriptional derepression, and mobilization of the element. In this study, to elucidate the mechanism of how VANC subtypes have diverged to bind specifically to their own target motifs in their cognate VANDAL subfamilies, we determined the crystal structure of VANC21 in complex with its target DNA at 2.0 Å resolution. The VANC structure adopts a globular novel fold with a Zn ion coordinated at the DNA-binding site. Interestingly, most DNA-interacting VANC residues are located in the loops but not in the conserved regions among VANC subtypes. This observation suggests that the high variability of DNA-interacting regions of VANC proteins brought about the co-evolution of VANCs and their target sequences. This rapid differentiation by co-evolution enabled VANDAL family TEs to proliferate while avoiding deleterious effects on host fitness. Therefore, our findings help to understand the adaptive evolutionary strategy for the survival of parasitic sequences.

The 2nd Asian Genetics Consortium Conference (AGCC 2025), entitled "Genetics in Asia: Heredity, Diversity, Discovery, and Beyond," was held in Numazu City, Shizuoka, Japan, from November 14-16, 2025. The conference was jointly organized by the Genetics Society of Japan as the leading host, together with the Genetics Societies and related organizations of the other five Asian countries (Korea, India, Singapore, Taiwan, and Thailand). A total of 72 participants attended, including 19 participants from six overseas countries and regions outside Japan. Invited speakers representing each country delivered lectures on cutting-edge research in genetics, its international significance, and future perspectives, followed by active and lively discussions. In addition, there were 30 poster presentations, mainly by young researchers, which stimulated vibrant scientific exchange. From among the presenters, one researcher received the Best Poster Award, and five researchers received Outstanding Poster Awards.

Neurotensin receptor 1 (NTSR1) is linked with poor prognosis in many tumors, including gastric cancer (GC). However, the exact mechanism by which NTSR1 affects GC anoikis in GC has not yet been clarified. Therefore, this project aimed to figure out the specific mechanism by which NTSR1 participated in GC anoikis. We herein assessed the expression of KLF5 and NTSR1 in GC tissues and the signaling pathways in which NTSR1 participated through the online bioinformatics website. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was employed to examine the expression of KLF5 and NTSR1. The CCK-8 kit was applied to detect the viability of GC cells under different treatments. Dual luciferase and chromatin immunoprecipitation (ChIP) experiments verified the binding relationship between KLF5 and NTSR1. The rate of fatty acid oxidation (FAO) was analyzed using a cell metabolism meter. The expression of FAO-related proteins was detected using the western blot (WB). The anoikis of cells in each group was detected using flow cytometry, anoikis apoptosis kit, and WB. We observed that knocking down NTSR1 repressed the vitality of GC cells, and elevated the anoikis rate and the expression of cleaved PARP and cleaved caspase 3 in GC cells. Moreover, high expression of NTSR1 up-regulated the expression of CTP1 protein in FAO and increased FAO levels, thereby suppressing the occurrence of anoikis in GC cells. The addition of the inhibitor of FAO (Etomoxir) reversed the above trends. In addition, KLF5 was highly expressed in GC, and KLF5 is an upstream transcription factor of NTSR1. Finally, KLF5 knockdown was verified to restore the repression of the FAO pathway and facilitate anoikis in GC cells by overexpressing NTSR1. In summary, our results suggested that KLF5 affects anoikis in GC cells by targeting NTSR1 to modulate the FAO pathway. Therefore, blocking the FAO pathway regulated by the KLF5/NTSR1 axis may become a new strategy for the treatment of GC.

In most eubacteria the initiator protein DnaA triggers chromosomal replication by forming an initiation complex at the origin of replication and also functions as a transcriptional regulator, coordinating gene expression with cell cycle progression. While genes regulated by DnaA are relatively well characterized in exponentially growing cells, its role in gene regulation during stationary phase remains insufficiently explored. Here, using the aquatic bacterium Caulobacter crescentus as a model, we show that C. crescentus DnaA (ccDnaA) acts as a repressor of the previously uncharacterized CCNA_00139 gene, which encodes a YifB family Mg chelatase-like AAA ATPase family protein of unknown function. Biochemical analyses reveal that ccDnaA forms multimers at this site, which may interfere with RNA polymerase access to the promoter by occupying overlapping binding sequences. Consistent with these findings, in exponentially growing C. crescentus cells the CCNA_00139 promoter is repressed in a ccDnaA-dependent manner. Notably, when cells enter stationary phase, CCNA_00139 promoter activity increases in parallel with ccDnaA clearance, supporting the idea that ccDnaA-mediated repression is relieved during this phase transition. Despite its regulated expression, deletion of CCNA_00139 did not result in any detectable growth, replication or DNA damage sensitivity phenotypes under the tested laboratory conditions, suggesting a possible role under specific environmental conditions. Given that this phase-dependent transcriptional switch may, in principle, apply to other uncharacterized ccDnaA-repressed genes, we infer that CCNA_00139, along with other such genes, form a regulatory network that supports quorum sensing or adaptation to growth phase transitions. We believe that these findings offer new insight into the potential role of bacterial DnaA in regulating gene expression in dormant or non-replicating cells across diverse bacterial species.

To explore the oncogenic mechanism of FOXM1 in the tumor microenvironment (TME) regarding triple-negative breast cancer (TNBC) promotion, the mRNA and protein levels of target genes in TNBC cells and their exosomes were detected by RT-qPCR and western blot. A co-culture model of TNBC cells and THP-1/M0 macrophages was established to detect the impact of co-culture on FOXM1 expression and the direction of macrophage polarization. A bioinformatics website was used to predict FOXM1 binding sites in the IDO1 promoter, which were further validated using dual-luciferase reporter and chromatin immunoprecipitation assays. Next, after erastin-induced ferroptosis, we conducted cell viability assays, apoptosis assays and other experiments to investigate whether the FOXM1/IDO1 axis regulates M2 macrophage polarization through ferroptosis. We found that FOXM1 was abundant in exosomes derived from TNBC cells, and that TNBC cells upregulated FOXM1 expression in THP-1 cells through exosomes to promote M2 macrophage polarization. Furthermore, FOXM1 upregulated IDO1 in M2-type tumor-associated macrophages (TAMs) by stimulating its transcription. Finally, FOXM1/IDO1 inhibited ferroptosis, promoting M2 macrophage polarization, thereby advancing TNBC progression. In conclusion, FOXM1 carried by TNBC cell-derived exosomes activated IDO1 transcription in TAMs to inhibit ferroptosis, promoting M2 polarization of TAMs and exerting carcinogenic effects.