9.9
CiteScore
7.1
Impact Factor
Dan-Yang Wang, Yin-Wei Wang, et al.
 doi: 10.1016/j.jgg.2026.03.023
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The gut microbiota is increasingly recognized as a regulator of reproductive health, yet its role in ovarian aging remains unclear. Here, we combine Mendelian randomization (MR) analysis with experimental validation to investigate the causal relationship between gut microbiota and ovarian aging. MR analysis identifies four microbial taxa significantly associated with age at natural menopause. In mouse models, germ-free mice exhibit accelerated ovarian functional decline, including reduced ovarian reserve and impaired folliculogenesis. Fecal microbiota transplantation (FMT) from young donors alleviates ovarian aging phenotypes, whereas FMT from aged donors exacerbates functional decline. Metagenomic analysis reveals species-level differences between young and ovarian-aging mice, with Parabacteroides johnsonii (P. johnsonii) enriched in young mice. Administration of P. johnsonii to middle-aged mice improves ovarian reserve, reduces follicular atresia, enhances granulosa cell proliferation, and decreases systemic inflammation. These findings highlight a causal role of the gut microbiota in ovarian aging and support microbiota-targeted interventions as a potential strategy to preserve ovarian function.
Jin-Dong Wang, Li-Jun Kan, et al.
 doi: 10.1016/j.jgg.2026.03.022
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Pre-harvest sprouting (PHS), caused by weak seed dormancy and environmental stimuli, leads to significant losses in both crop yield and grain quality. Breeding crop cultivars with enhanced PHS resistance represents a promising strategy to address this challenge. However, limited useful genetic resources has hindered the progress in rice molecular breeding. Through screening of a rice mutant library, we identify the ethylene response factor115 (erf115) mutant, which exhibits enhanced PHS resistance. Genetic analysis reveals that ERF115 functions as a negative regulator of seed dormancy. Mechanistic assays show that the E3 ubiquitin-protein ligase Grain Width and Weight 2 (GW2) interacts with and ubiquitinates ERF115, thereby promoting its proteasomal degradation. Accordingly, gw2 mutants display increased PHS susceptibility. ERF115 also interacts with the transcription factor SLR1-like 2 (SLRL2) and represses its transcriptional activation activity, consequently reducing the expression of the dormancy gene Mother of FT and TFL1 like 2 (MFT2). Haplotype analysis identifies three major ERF115 haplotypes (HapI–HapIII), among which ERF115HapI represents an elite allele associated with reduced PHS. Collectively, our findings reveal a GW2–ERF115–SLRL2 regulatory module that integrates ubiquitin-mediated regulation and hormone signaling to fine-tune rice seed dormancy, providing valuable genetic resources for breeding PHS-resistant rice varieties.
Yuyu Wang, Rongrong Li, et al.
 doi: 10.1016/j.jgg.2026.03.021
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Seed size is a key determinant of cereal grain yield, but natural variations in defective-kernel genes have rarely been applied in maize breeding. Here, we report the positional cloning of maize Miniature5 (Mn5), which encodes a mitochondrial-targeted P-class pentatricopeptide repeat (PPR) protein. Further analysis shows that a missense mutation of mn5, Mn5Val109, presents in maize populations and correlates with reduced seed size. The Mn5Val109 variant exhibits compromised function in the mn5-ref mutant, failing to trans-splice mitochondrial nad1 intron1, drastically reducing the abundance and activity of respiratory complex I, accompanied by disorganized mitochondrial cristae. Mn5 directly binds to domain IV of the pre-nad1.1 transcript. Notably, this binding site is located downstream of the previously presumed 3′-terminus bound by MITOCHONDRIA STABILITY/PROCESSING PPR FACTOR1 (MSP1), thus redefining the 3′-end of the nad1.1 pre-RNA. Furthermore, Mn5 physically interacts with the maturases ZmnMAT1 and ZmnMAT3, as well as the PPR proteins PPR-SMR1 and SPR2, which are broadly involved in organellar group II intron splicing. Together, our results suggest that Mn5 recruits maturases and PPR proteins to form spliceosomal complexes responsible for the trans-splicing of nad1 intron1. Importantly, natural variations in Mn5 confer differences in seed size control, offering potential for breeding high-yield maize varieties.
Hongling Zhou, Weixue Mu, et al.
 doi: 10.1016/j.jgg.2026.03.011
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Epigenetic inheritance is fundamental to human development and disease, yet the mechanisms governing the transmission of DNA methylation across generations remain incompletely understood. In this study, we performed haplotype-resolved, whole-genome DNA methylation profiling in a healthy three-generation Chinese family, leveraging high-depth Oxford Nanopore Technologies (ONT) and PacBio HiFi long-read sequencing, anchored to a proband-specific telomere-to-telomere (T2T) genome assembly. We observed globally conserved bimodal methylation landscapes across all individuals and generations. Stratified analyses revealed clear functional compartmentalization of methylation marks, characterized by distinct hypomethylation in centromeres and hypermethylation in retrotransposons and repetitive elements. Chromosome-resolved analysis of ribosomal DNA (rDNA) arrays demonstrated a domain-specific methylation pattern with hypomethylation in the transcriptional core and hypermethylation in the intergenic spacer, with evidence for age-associated epigenetic drift in the transcriptional core domain. Through de novo identification and validation, we mapped 23 high-confidence imprinting control regions (ICRs) showing robust parent-of-origin-specific methylation, all overlapping known imprinted genes and enriched for regulatory element signatures. Haplotype-resolved X chromosome analysis further uncovered sex- and allele-specific methylation patterns linked to X inactivation dynamics. Together, this pedigree-scale, high-resolution study delineates the landscape and principles of intergenerational DNA methylation inheritance, revealing both conserved and dynamic features shaping the human epigenome.
Huimin Ren, Hong Liu, et al.
 doi: 10.1016/j.jgg.2026.03.018
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Global warming intensification elevates heat stress to one of the major threats to crop productivity. This review synthesizes recent advances in understanding the mechanisms governing plant responses to both moderate and acute heat stress, with a focus on the integration of epigenetic regulation and signaling networks that underpin thermal adaptation. This review highlights how transcription factors PHYTOCHROME-INTERACTING FACTOR 4 (PIF4, during thermomorphogenesis) and HEAT SHOCK FACTOR A1s (HSFA1s, in heat shock responses) orchestrate plant adaptive growth through crosstalk among light, circadian, and hormone signaling pathways. Importantly, epigenetic mechanisms, including histone variant H2A.Z dynamics and histone modification reprogramming, function as central regulators of thermal plasticity. Key among these processes are HSFA2-mediated chromatin remodeling and small interfering RNA (siRNA)-dependent control of transgenerational thermomemory. Despite this progress, fundamental questions persist regarding temperature sensing, HSFA1s activation dynamics, and stress signal integration. Multi-omics and synthetic biology approaches are proposed to be pivotal in deciphering conserved principles of plant thermal resilience, ultimately providing a theoretical foundation and molecular breeding strategies for climate-smart crops.
Shuhao Liu, Ying Shen, et al.
 doi: 10.1016/j.jgg.2026.03.020
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