bioRxiv Science⌕ Search
Home/Archive/bioRxiv

bioRxiv · 10.64898/2026.01.17.700121

Simultaneous selection for yield and stability in cassava (Manihot esculenta Crantz) under optimum condition in Nigeria

Oyebode, O. G.·Olayiwola, R.
View original source ↗Export metadata ↓

Abstract

High yield and stability of performance across environments are required for success in agricultural systems. Selection of high yielding and stable genotypes is always hindered by Genotype by environment interaction (GEI). Hence plant breeders have proposed diverse methods to help increase their efficiency of selection in multi environment yield trials. The aim of this experiment was to identify and select high yielding and stable cassava genotypes using to GGE biplot and Yield selection index (YSi) techniques and to determine the efficiency of the techniques. 24 hybrids and 2 checks were tested across five locations in Nigeria using the randomized complete block design with 4 replications. ANOVA provided clear evidence of GEI (P<0.001) for dry root yield. 23 of the hybrids showed 10% to 83% economic improvement over the best check variety. GGE biplot identified genotypes TMS-IBA090574, TMS-IBA090521, TMS-IBA090590 and TMS-IBA090576 as high yielding and stable, while YSi selected 14 genotypes TMS-IBA090454, TMS-IBA090504, TMS-IBA090506, TMS-IBA090509, TMS-IBA090521, TMS-IBA090523, TMS-IBA090536, TMS-IBA090564, TMS-IBA090574, TMS-IBA090576, TMS-IBA090581, TMS-IBA090590, TMS-IBA090597 and TMS-IBA090609. Six of these genotypes (TMS-IBA090523, TMS-IBA090536, TMS-IBA090574, TMS-IBA090581, TMS-IBA090506, TMS-IBA090521) were marked as unstable by the Shuklas stability variance which indicates a weakness of YSi. The two techniques identified TMS-IBA090590 and TMS-IBA090576 as high yielding and stable genotypes. These two clones performed above average in at least four of the five locations used for evaluation. The genotypes jointly selected by both methods may therefore be released to increase the productivity of the crop in Nigeria and comparable agro ecology.

Explore related subjects

geneticsPreprint

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Oyebode, O. G., Olayiwola, R.. 2026-01-21. Simultaneous selection for yield and stability in cassava (Manihot esculenta Crantz) under optimum condition in Nigeria. https://doi.org/10.64898/2026.01.17.700121

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

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↗
bioRxiv2026

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↗