Search bioRxiv⌕ Search
Home/Archive/bioRxiv

bioRxiv · 10.1101/2025.05.22.655537

Multivariate Analysis for Agro-Morphological and Quality Traits in Groundnut (Arachis hypogaea L.) Genotypes in Eastern Ethiopia

Dama, D. B.
View original source ↗Export metadata ↓

Abstract

It is imperative to study the level of genetic variability available in the existing groundnut genotypes due to the fact that, the aim of groundnut breeding programs across the world is to develop new varieties that meet the needs of growers, processors, consumers, and overall market demands. The present study was carried out to assess the extent of genetic variability among groundnut genotypes for agro-morphological and quality traits. Thirty-six groundnut genotypes were evaluated in a 6 x 6 simple lattice design during 2023 post-rainy season under irrigation at Dire Dawa, the research station of Haramaya university, Ethiopia. Data were collected on kernel yield and other morphological traits, oil content and oil yield. The data on traits were subjected for principal component (PC) values, clustering and Euclidean distance. In this study, the first six Principal Components Analysis (PCA) found to be significant and accounted for 74.51% of the total variation in which the first principal component (PC1) and the second principal component (PC2) contributed more to the variation. Those 36 genotypes were grouped into six major clusters and the dendrogram showed that cluster I, II, III, IV, V and VI included 6, 9, 8, 5, 7 and 1 numbers of genotypes in that order. Euclidean distance ranged from 2.45 to 8.54 with the mean, standard deviation and coefficient of variation of 5.44, 1.17 and 21.56%, respectively. Based on the result of the current study, there were variations of genetic distances among genotypes, Gv17 and Gv28, Gv3 and Gv23, Gv3 and Gv30, Gv15 and Gv17, Gv22 and Gv28, and Gv3 and Gv34 which could be exploited through hybridization for cultivar development in groundnut breeding programs in Ethiopia. Therefore, these genotypes are recommended as excellent candidates for further breeding and variety development.

Explore related subjects

geneticsPreprint

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Dama, D. B.. 2025-05-27. Multivariate Analysis for Agro-Morphological and Quality Traits in Groundnut (Arachis hypogaea L.) Genotypes in Eastern Ethiopia. https://doi.org/10.1101/2025.05.22.655537

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

KEEP EXPLORING

Related preprints

bioRxiv2026

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↗
bioRxiv2026

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↗
bioRxiv2026

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↗