Search bioRxiv⌕ Search

bioRxiv · 10.64898/2026.10.16.757273

Phenomic selection enables nursery screening for field performance in maize and pea

Abstract

Due to economical constraints, breeding programs eliminate most selection candidates at early stages, before their productivity can be evaluated in field trials. Genomic selection partially overcomes this limitation by enabling early prediction of field performance, but its implementation requires large-scale recurrent genotyping that remains inaccessible for many species and breeding programs. Phenomic selection offers a promising alternative by replacing genotyping with inexpensive high-dimensional phenotyping data. However, previous applications have focused on predicting genotypes already evaluated in field trials. We investigated whether phenomic data acquired by unoccupied aerial vehicles (UAVs) from nursery-grown genotypes can be used to predict their performance in field trials. We validated this nursery-screening approach in maize and pea, two species with contrasting biology and canopy structures, supporting its potential transferability to other species. In the most challenging scenarios, average accuracies for yield-related traits were between 0.36 for maize and 0.40 for pea. Simulations indicated that these accuracies can support substantial nursery culling while limiting the risk of discarding superior genotypes. This proof of concept demonstrates that UAV-based phenomic selection can predict the field performance of nursery-grown genotypes without genotyping the selection candidates.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Rincent, R., Hamon, Q., Garcia Dias, A., Ecarnot, M., Nunes, L., Bauland, C., Dai, P., Comar, A., Touzy, G., Barthes, F., Gouache, D., Le Mener, A., Goudemand, E., Moreau, L.. 2026-10-16. Phenomic selection enables nursery screening for field performance in maize and pea. https://doi.org/10.64898/2026.10.16.757273

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

KEEP EXPLORING

Related preprints

The Alzheimer's disease-associated rs28834970 variant in PTK2B impairs electrical activity and regulates Tau phosphorylation and APP processing in human neuronal cultures

Background: Genome-wide association studies have identified the PTK2B gene, which encodes Proline-rich tyrosine kinase 2 (PYK2), as a genetic risk factor for Alzheimer's disease (AD). However, its role in AD aetiology remains to be understood, as a complex contribution to amyloid {beta} (A{beta}) toxicity, tauopathy and neuronal dysfunction is suggested by contradictory evidence. Determining how the causal variant among AD-associated PTK2B variants impairs PYK2 function to trigger AD hallmarks could bring clarification. Methods: We combined in silico prediction tools with luciferase reporter assays in neuroblastoma cells to prioritize potential AD-associated PTK2B functional variants. We generated isogenic KOLF2.1J induced pluripotent stem cells (iPSCs) carrying the most relevant functional variant using CRISPR-Cas9 and differentiated them into human neuronal cultures (hNCs). We assessed PYK2 expression via immunoblotting, performed transcriptomic profiling using RNA-sequencing, analyzed neuronal network activity via multielectrode array (MEA) recordings, quantified synaptic density through immunocytochemistry in microfluidic devices, and assessed Tau phosphorylation and amyloid-precursor protein (APP) metabolism. Results: The rs28834970 regulatory variant was identified as the most functionally relevant in our model, with the C risk allele promoting transcription factor C/EBP{beta} binding within a cis-regulatory element. In hNCs, the homozygous rs28834970 CC genotype reduced total PYK2 levels by more than 80%, while increasing the proportion of phosphorylated (activated) PYK2. Transcriptomic analysis revealed 724 downregulated and 113 upregulated gene sets, with altered expression of genes involved in extracellular matrix organization, cytoplasmic translation and neurotransmitter secretion. MEA recordings showed reduced network recruitment and altered burst organization. Immunocytochemistry in microfluidic devices consistently revealed that rs28834970 impacts dendritic development and postsynaptic maturation. The risk genotype significantly elevated Tau phosphorylation at pathological sites (Thr181, Thr217, Thr231, Ser202-Thr205, Ser396-Ser404), and enhanced APP processing, resulting in decreased levels of APP and CTF but increased levels of sAPP, sAPP{beta} and A{beta}. Conclusion: The rs28834970 C risk allele mechanistically links AD susceptibility to downregulation of PTK2B/PYK2 expression and to the increase in Tau pathology and A{beta} levels while compromising synaptic structure and function.

genetics↗

Human infection with an ape Plasmodium vivax-like parasite

An unusually divergent Plasmodium vivax parasite was reported in a Swedish patient with recent travel. Using whole-genome sequencing, we show that the infection was caused by a strain of ape P. vivax-like, providing evidence of the zoonotic potential of these parasites that infect wild gorillas and chimpanzees in central Africa.

genetics↗

Preclinical Development and Safety of Laterally Spreading Dual AAV.SPR-MYO7A Vectors for the Treatment of Usher Syndrome Type 1B

Usher syndrome type 1B (USH1B), caused by mutations in MYO7A, is the most severe form of Usher syndrome and accounts for more than 50% of USH1 cases. Affected patients are born profoundly deaf with vestibular dysfunction and develop progressive retinitis pigmentosa, for which no approved treatment exists. The MYO7A coding sequence exceeds the packaging capacity of adeno-associated virus (AAV), the gold standard vector for retinal gene therapy. To overcome this, we developed dual AAV hybrid and overlap platforms to reconstitute full-length MYO7A expression in photoreceptors and retinal pigment epithelium. Modification of cDNA split points, and reduction of non-coding sequence yielded optimized vector pairs that produced higher full-length MYO7A levels with substantially reduced truncated protein. Packaging in the laterally spreading AAV.SPR capsid enabled supraphysiological MYO7A expression in cynomolgus macaques at macular and distal retinal sites without requiring foveal detachment, an important safety consideration for USH1B patients with remaining central vision. A six-month GLP toxicology study confirmed that ATSN-301, an AAV.SPR-based dual vector reconstituting MYO7A driven by the smCBA promoter, was well tolerated at all doses, with a No Observed Adverse Effect Level established at 1.2E11 vg/eye, supporting its clinical advancement for USH1B.

genetics↗