bioRxiv Science⌕ Search
Home/Archive/bioRxiv

bioRxiv · 10.1101/2025.07.23.666412

Genetic enhancement of inbred lines through pre-breeding in maize

Neelam, S.·Oruganti, S.·Bhoga, J.·Mallela venkata, N. K.·Gangadhar, C. K.·Satturu, V.
View original source ↗Export metadata ↓

Abstract

The improvement in the genetic yield potential of maize has led to the development of an extremely large number of maize cultivars across almost all maize-growing countries in the world. In the process, the genetic diversity in the modern maize cultivars has gradually narrowed down. To improve the genetic diversity, there is a need to undertake pre-breeding through wide-hybridization between inbred lines and their wild species, namely Zea mays ssp. Parvigluimis (WS-5) and Zea luxurians (WS-1). In the present study, 69 elite inbred lines were crossed with two wild relatives of maize, Z. mays ssp. Parviglumis and Z. luxurians. The resulting hybrids of wide hybridization showed typical wild species characters like tillering, prolificacy on main tiller and side tillers, and ear characters. This shows the introgression of characters from wild species. Combining ability analysis revealed the presence of a significant amount of variability among parents and crosses for most traits under study. Z. luxurians was a good general combiner for all the traits except tassel length, anthesis silking interval, and days to 75% dry husk based on the GCA effects. Whereas lines, IC0621049 and IC0621565, were good general combiners for all the traits except days to 75% dry husk. Among the crosses, highly significant SCA effects in the desired direction were shown by PFSR-3 x WS-5, EC618215 x WS-1, and IC213122 x WS-1 for plant height, ear diameter, no. of kernel rows per ear, no. of kernels per row, ear weight, and grain yield per ear. Molecular analysis also confirmed the genuine nature of hybrids. Cluster analysis classified all the parents involved in the crosses into two groups, with most of the inbred lines grouping with WS-5, revealing that most of the inbred lines were closely related to WS-5 as compared to WS-1. This may be the reason for the development of more successful crosses with WS-5 as compared to WS-1.

Explore related subjects

geneticsPreprint

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Neelam, S., Oruganti, S., Bhoga, J., Mallela venkata, N. K., Gangadhar, C. K., Satturu, V.. 2025-07-26. Genetic enhancement of inbred lines through pre-breeding in maize. https://doi.org/10.1101/2025.07.23.666412

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↗