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Murigneux, A.

Publications and source records attributed to Murigneux, A..

2 recordsLinked to original sources
bioRxiv2026

Identification of heterotic group-specific haplotypes and impact of residual inbreeding on grain yield of maize elite hybrids

Modern hybrid maize (Zea mays L.) breeding programs are based on the management of distinct complementary heterotic groups to maximize heterosis in high-performing hybrids. This practice lowers shared genetic segments and increases divergence between groups to limit inbreeding in hybrids. However, most breeding programs have not always enforced strict separation between heterotic groups in the past. Competitor commercial hybrids were notably a common elite germplasm source for inbred development, which would diminish divergence between groups. This study proposes a new haplotype-based approach to assess hybrids residual inbreeding based on parental similarity. The new haplotype method has a stronger significant negative effect on hybrids grain yield than raw SNP data. Evaluation of modern experimental hybrids uncovered related inbreds contributing to superior rates of residual inbreeding. Analysis of these inbreds revealed haplotype transfers between heterotic groups, originating notably from the use of a Stiff Stalk-Iodent commercial hybrid as breeding starts material in both Stiff Stalk and Non-Stiff Stalk breeding populations. The introduction of this intergroup parent generated heterotic-group-specific haplotype migration between crossing pools. These fragments caused significant genome-wide residual inbreeding in experimental hybrids across selection cycles. This study highlights the necessity for accurate evaluation of external sources of diversity to minimize haplotype transfers and admixture between crossing pools. We demonstrate the consequences of using commercial hybrids in inbred development, particularly regarding residual inbreeding, and their effects on hybrid performance. Insights from these results can assist breeders in optimizing the choice of parents for introducing genetic diversity in a reciprocal recurrent selection scheme. KEY MESSAGEHaplotype-based hybrids parental similarity better predicts grain yield than marker-based identity-by-state. Utilization of commercial hybrids as breeding start material resulted in higher hybrid residual inbreeding even after several selection cycles

genetics↗
bioRxiv2026

The elongation of Mest transcript into MestXL sustains, but does not initiate, the maternal allele bias of its convergent gene Copg2 during neurogenesis

Precise gene dosage control is critical for establishing cellular identity and development, especially for imprinted genes, where dosage imbalances are linked to severe pathologies such as neurodevelopmental disorders. The Mest/Copg2 imprinted locus is a paradigm for this fine-tuned regulation. While Mest is constitutively expressed from the paternal allele, Copg2 expression shifts from biallelic to a maternal allele bias specifically during neural differentiation, a transition proposed to involve transcriptional interference mediated by the long Mest isoform, MestXL, which extends into the Copg2 locus. However, the mechanisms underlying this allelic switch, and whether factors beyond MestXL contribute, are elusive. To address this, we employed a stem cell-based brain organoid model, integrating multi-omic analyses, 3D chromatin structure mapping, and functional approaches to dissect the regulatory events governing the induction and maintenance of Copg2 maternal allele bias throughout neural lineage specification. Our findings challenge the prevailing model by demonstrating that the maternal allele bias of Copg2 during neural differentiation is not solely driven by MestXL-mediated transcriptional interference. Instead, our data support a temporal and neural stage-specific two-step mechanism: putative enhancer-driven activation of the maternal allele in neural progenitor cells is followed by MestXL-dependent repression of the paternal allele in neuron-enriched stages. This uncovers an unexpected layer of complexity in the regulation of imprinted gene dosage during brain development, with profound implications for understanding the molecular underpinnings of neurodevelopmental disorders.

molecular biology↗