Search bioRxiv⌕ Search

bioRxiv · 10.64898/2026.01.22.701136

Genomic and pedigree-based approaches to predict parental breeding values for nut and kernel traits in almond (Prunus dulcis Mill. D. A. Webb)

Abstract

The self-incompatibility, perennial growth habit, large tree size, and long juvenility present challenges in applying traditional breeding approaches in almond (Prunus dulcis Mill. D. A. Webb). Moreover, nut and kernel traits in almond are mainly controlled by a large number of small-effect quantitative trait loci (QTLs) and improving complex traits through conventional breeding approaches is slow and often inefficient. Genome-wide selection represents a promising strategy to enhance the efficiency of cultivar identification and selection of superior parents in almond breeding programs by estimating the breeding values (BVs) at early maturity. The main aim of this study was to implement genomic (GBLUP) and pedigree-based (ABLUP) prediction approaches to estimate BVs to identify the superior parental candidates for improving nut and kernel traits in almond. Here, we estimated BVs for nine traits that are commonly used in the primary evaluation stage of the almond breeding using genomic data from 61 parents and phenotypic data of 15,281 progeny derived from 205 unique families. Breeding values obtained from both approaches showed a strong correlation (r [≥] 0.94) for all traits except shell seal (r = 0.87). The population structure analysis conducted using high-quality 90K single nucleotide polymorphisms (SNPs) indicated clear separation of the Californian, European and some old Australian almond cultivars, with considerable admixture across some cultivars. Following further validation, both prediction approaches could be useful in early identification of superior candidates. The slightly higher breeding values obtained using the GBLUP compared to the ABLUP approach suggest that accounting for within-family variations and realised genomic relationships can enhance prediction accuracy, reliability, and overall genomic prediction performance in almond.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Goonetilleke, S., Wilkinson, M. J., Wirthensohn, M. G., Collins, C., Furtado, A., Henry, R. J., Hardner, C.. 2026-01-24. Genomic and pedigree-based approaches to predict parental breeding values for nut and kernel traits in almond (Prunus dulcis Mill. D. A. Webb). https://doi.org/10.64898/2026.01.22.701136

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↗

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↗

Innate immune stress pathway activation underlies heterochromatin dysfunction pathology

Heterochromatin loss disrupts nuclear architecture, gene regulation and repetitive element silencing, and is associated with diverse human diseases. However, mechanisms linking heterochromatin dysfunction to pathological phenotypes remain unclear. Using genetic interaction screening and genomic analyses in C. elegans, we identify secondary activation of the Intracellular Pathogen Response (IPR), an innate immune stress pathway, as a major contributor to heterochromatin mutant phenotypes. Constitutive IPR activation phenocopies slow growth and indirect transcriptional changes observed in these mutants. Depletion of genetic enhancers further increased, whereas suppressor RNAi attenuated IPR activation, with direct heterochromatin targets remaining substantially deregulated. Notably, many suppressors encode active chromatin components, and mild reduction of RNA polymerase II activity ameliorates growth defects in C. elegans HP1 mutants and human HP1-deficient cells. Our findings reveal secondary stress response activation as an important mechanism linking heterochromatin dysfunction to pathology and identify transcriptional dampening as a potential therapeutic strategy for mitigating these effects.

genetics↗