Search bioRxiv⌕ Search

bioRxiv · 10.1101/2025.05.18.654744

Exploring the genetic factors of nitrogen use efficiency in potato

Abstract

Nitrogen is an essential nutrient for plants, used by farmers to increase the yield of the crops. However, this practice increases greenhouse gases, negatively affecting the environment. Nitrogen Use Efficiency (NUE) is a trait that is beginning to be studied in some model species and in cereals due to its complex and novel trait nature. In potatoes, the information is scarcer. The study of NUE at the genetic level, based on a diverse population in potato materials, will contribute to the understanding of the genetic architecture of the trait. This research evaluated NUE in a Solanum tuberosum diploid potato genetic diversity panel from the Phureja group. The characterization of the trait was carried out in substrate conditions, for low and high levels of nitrogen for both the vegetative and the reproductive phase. Eighteen variables associated with NUE were measured, nine under low nitrogen and nine under high nitrogen conditions. A GWAS was conducted, and a total of 21 QTNs were identified as strongly associated with 11 phenotypic variables related to NUE in potato, along with a repertoire of 750 candidate genes associated with the trait. This research aimed to establish the basis for understanding the genetic architecture of NUE in Solanum tuberosum. Likewise, the knowledge derived is expected to be useful for plant breeding programs that begin to improve this trait.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Mendoza-Bustamante, M. A., Jimenez-Medrano, A. N., Soto-Sedano, J. C., Delgado-Nino, M. C., Magnitskiy, S., Ligarreto-Moreno, G. A., Mosquera Vasquez, T.. 2025-05-23. Exploring the genetic factors of nitrogen use efficiency in potato. https://doi.org/10.1101/2025.05.18.654744

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

OPA1 controls mitochondrial dysfunction-driven liver fibrosis in MASLD

Progressive hepatic fibrosis is the principal determinant of morbidity and mortality in metabolic dysfunction-associated steatotic liver disease and steatohepatitis (MASLD/MASH). Mitochondrial dysfunction is a hallmark of MASH, and the release of mitochondrial damage-associated molecular patterns (mito-DAMPs) from injured hepatocytes can promote fibrosis. However, how mitochondrial dynamics and quality control shape the fibrotic response in MASLD/MASH remains unclear. Here, through large-scale genomic analyses of mitochondrial genes governing mitophagy, fusion and fission in human MASLD, with a power-equivalent sample size of approximately 700,000 individuals, we identify a strong association between hepatic fibrosis and the mitochondrial fusion factor dynamin-like GTPase optic atrophy 1 (OPA1). OPA1 transcripts and protein abundance in the liver epithelium were progressively dysregulated with advancing fibrosis. In mice, hepatocyte-specific OPA1 loss alone was sufficient to induce hepatic stellate cell activation and fibrosis in zone 3, promoted the release of mito-DAMPs into the circulation and exacerbated fibrosis in experimental MASH. These findings identify OPA1 as a central regulator of the hepatic fibrotic response and connect defective mitochondrial homeostasis to mito-DAMP release, hepatic stellate cell activation and fibrosis in MASLD.

genetics↗

Mechanism-selective deep mutational scanning distinguishes ERCC2 disease phenotypes

Pathogenic ERCC2 variants cause xeroderma pigmentosum (XP), trichothiodystrophy (TTD) or both, yet variant effect scores are usually interpreted only as measures of pathogenicity rather than of which disease mechanism is disrupted. XPD, the ERCC2-encoded TFIIH subunit, functions in both nucleotide excision repair and transcription. Using yeast complementation deep mutational scanning, we measured the effects of nearly all XPD amino acid substitutions. The assay was mechanism-selective: it preferentially reported transcription-associated function, with pronounced intolerance at the p44 interface, whereas many substitutions affecting DNA binding and helicase activity retained near-wild-type fitness. Accordingly, TTD variants had much lower fitness than XP variants. Computational predictors discriminated pathogenic from benign variants similarly across phenotypes, but the DMS distinguished XP from TTD variants better than all 73 predictors tested. Phenotype-specific ACMG/AMP calibration provided evidence in both directions for TTD but mainly pathogenic evidence for XP. Thus, the selectivity of functional assays, often viewed as a limitation, can reveal disease mechanisms and support phenotype-aware variant interpretation.

genetics↗

Temporal control of mitochondrial mutagenesis reveals the fate of mtDNA mutations with age

Mutations in the mitochondrial genome (mtDNA) play a critical role in the aging process and a wide variety of age-related diseases. However, it remains unclear when the mutations that drive physiological decline arise. To answer this question, we generated a new mouse model in which mitochondrial mutagenesis can be confined to a defined window of time. Surprisingly, we found that mutations that arise during the first two months of life are sufficient to drive a wide variety of age-related pathologies, and that the severity of this pathology is broadly regulated by distinct, tissue-specific selective pressures that control the fate of mtDNA mutations with age. Further, we found that selection against deleterious variants can be modulated by manipulation of mitochondrial fusion in vitro and in vivo. These observations raise the possibility that in some tissues, the pace of aging is pre-determined by events that occur early in life and that interventions targeting mitochondrial fusion may be able to slow down or reverse the expansion of these pathogenic variants. These results carry far-reaching implications for strategies aimed at preventing or delaying age-related decline.

genetics↗