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Hong Pan

Publications and source records attributed to Hong Pan.

3 recordsLinked to original sources

Transmission dynamics and driving mechanisms of antibiotic resistance genes through a chronosequence of saline-sodic rice cultivation.

Rice cultivation reclaims saline-sodic soils and improves fertility, but may also promote antibiotic resistance genes (ARGs) accumulation and horizontal transfer, posing ecological risks. This study investigated long-term co-evolution of soil properties, microbial communities, ARGs, and mobile genetic elements (MGEs) across a 1-78 year cultivation chronosequence in saline-sodic fields. Results indicated that prolonged cultivation effectively alleviated soil salinization and increased fertility. Microbial communities shifted directionally, with functional taxa enriched, while opportunistic pathogen-containing genera peaked during 5-20 years. ARGs abundance and diversity increased markedly after five years and peaked at 10-20 years. Multidrug efflux pump genes persisted throughout the chronosequence, whereas aminoglycoside resistance genes declined after 30 years. MGEs activity increased over time and was significantly correlated with key ARGs. Path analysis identified improved soil properties as the primary direct driver of ARGs accumulation, while cultivation-induced declines in microbial diversity indirectly promoted ARGs dissemination by weakening the community's suppression of MGEs-mediated horizontal transfer. Collectively, long-term rice cultivation not only ameliorated saline-sodic soils but also created a dynamic, stage-specific resistome, with the 5-20 year period representing a critical risk window for ARGs propagation. These findings highlight the need to integrate ARGs monitoring into soil health assessments for sustainable management of reclaimed saline-sodic lands.

Oryza

CasY7: An optimized Cas12i system for enhanced genome editing in monocot crops.

The CRISPR-Cas12 family nucleases, particularly the Cas12i subtypes, are considered promising alternatives to Cas9 for genome editing in plants. We previously developed a new Cas12i variant, CasY7, which has been successfully applied in clinical trials; its performance in plants remains to be investigated. Initial testing in stable transgenic maize and rice showed that the codon-optimized CasY7 (pCasY7e1) achieved average editing efficiencies of 58.7% and 62.3% across five target sites, respectively, outperforming the typical Cpf1 (pCpf1) control that targets the same sites. To further enhance activity, we fused T5 exonuclease to CasY7 (pCasY7e2), which shifted mutation profiles toward larger deletions, and subsequently integrated an MS2 aptamer into the crRNA scaffold (pCasY7e3). The optimized pCasY7e3 system increased editing efficiencies to 87.7% in maize and 82.9% in rice-approximately 2.7-fold higher than pCpf1. We further demonstrated multiplexed editing in maize, generating biallelic dwarf mutants, and validated functionality in hexaploid wheat with editing efficiencies up to 58.8%. Overall, our comprehensive validation across 942 transgenic plants confirmed robust editing in maize, rice, and wheat, establishing CasY7 as a high-efficiency addition to the CRISPR toolkit.

Zea mays

Genome-wide association study of adolescent-onset depression.

Adolescent depression is a heritable psychiatric condition with rising global prevalence and severe long-term outcomes, yet its biological underpinnings remain poorly understood. We conducted the first genome-wide association study of adolescent-onset depression, comprising 102,428 cases (diagnosis or clinical symptom thresholds) and 286,911 controls, including diverse ancestries. Cross-ancestry meta-analysis identified 52 independent variants across 17 loci; European-only analysis found 61 variants at 29 loci, with a SNP-based heritability of 9.8%. Comparative analyses revealed two genes unique to adolescent-onset versus lifetime depression, enriched in neuronal subtypes, and two genes as potential drug repurposing targets. Polygenic scores were associated with adolescent-onset depression across ancestries, persistent depression trajectories, more severe outcomes, as well as reduced cortical volume, surface area and white matter integrity. Genetic correlation and Mendelian randomisation analyses support shared genetic liability and causal links with early puberty and modifiable health and behavioural risk factors. These findings uncover novel genetic loci and refine biological pathways underlying adolescent-onset depression, revealing age-specific mechanisms and early intervention opportunities.

Journal Article