# Metabolic engineering of soybean for improving grain quality for animal consumption

**Authors:** João Matheus Kafer, João Vitor da Silva, Suéllen Rosa de Almeida Polizeli, Rodrigo Thibes Hoshino, Juliana da Rosa, Elibio Leopoldo Rech Filho, Alexandre Lima Nepomuceno, Liliane Marcia Mertz-Henning

PMC · DOI: 10.3389/fpls.2026.1738805 · Frontiers in Plant Science · 2026-02-18

## TL;DR

This paper reviews how metabolic engineering can improve soybean grain quality for animal feed by reducing harmful compounds and increasing protein content.

## Contribution

The paper highlights recent advances in using gene editing and metabolic engineering to optimize soybean for animal consumption.

## Key findings

- Silencing genes like CIF1 and AIP2 increases seed protein content.
- Editing SWEET10a and SWEET10b modulates the oil-protein balance in soybean.
- Inactivating genes related to antinutritional factors reduces phytate and protease inhibitors.

## Abstract

Soybean is one of the main sources of vegetable protein used in animal feed, but its nutritional value is limited by the presence of antinutritional factors, such as protease inhibitors (Kunitz and Bowman–Birk), lectins, phytic acid, raffinose family oligosaccharides (RFOs), and saponins, which reduce the digestibility and absorption of nutrients. In recent decades, advances in metabolic engineering and functional genomics have allowed the targeting of biochemical pathways to increase the content and quality of proteins while simultaneously reducing these undesirable compounds. This work reviews the main progress achieved through transgenesis, induced mutagenesis, and precision gene editing, highlighting the role of tools such as RNAi, CRISPR/Cas9, and AlphaFold2-guided gene editing in modifying genes involved in carbon and nitrogen metabolism and storage proteins. Recent studies demonstrate that the silencing of negative regulatory genes, such as CIF1 and AIP2, can elevate the protein content of seeds, while the editing of sugar transporters SWEET10a and SWEET10b allows the modulation of the oil-protein balance. Simultaneously, the inactivation of genes related to antinutritional factors has significantly reduced the expression of compounds such as phytate and protease inhibitors. The integration of new approaches, such as promoter engineering and Prime Editing, promises to further enhance the precision of genetic modifications, minimizing pleiotropic effects. Taken together, these strategies consolidate metabolic engineering as a promising tool for the development of soybean cultivars with higher protein content and quality, and with lower content of antinutritional factors, optimizing their use in animal feed

## Linked entities

- **Genes:** cif-1 (COP9/Signalosome and eIF3 complex-shared subunit 1) [NCBI Gene 177236], WWP2 (WW domain containing E3 ubiquitin protein ligase 2) [NCBI Gene 11060], LOC110631146 (bidirectional sugar transporter SWEET10) [NCBI Gene 110631146]
- **Chemicals:** phytate (PubChem CID 890)

## Full-text entities

- **Genes:** thioredoxin [NCBI Gene 547759], TOC1 [NCBI Gene 100271889], Gy1 [NCBI Gene 547901], LE1 (lectin) [NCBI Gene 100818710] {aka Agglutinin, SBA}, MIPS (myo-inositol-3-phosphate synthase) [NCBI Gene 547604] {aka GmMIPS1, INPS, MIPS1}, COL2a (CONSTANS-like 2a) [NCBI Gene 100301885] {aka COL1a, CONSTANS}, GY2 (glycinin subunit G2) [NCBI Gene 547900] {aka A2B1a, glycinin}, Glycinin [NCBI Gene 732636], BBI (Bowman-Birk proteinase inhibitor) [NCBI Gene 548083], STS [NCBI Gene 100815922], GOLS (galactinol synthase) [NCBI Gene 548050] {aka GmGolS}, Lectin [NCBI Gene 547726], Gy7 [NCBI Gene 547611], IPK2 [NCBI Gene 100127407], IPK1 [NCBI Gene 100127406], alpha-amylase [NCBI Gene 100792499], P34 [NCBI Gene 548062], KTI3 (Kunitz trypsin inhibitor) [NCBI Gene 547831] {aka KTi, Ti-a, Ti-b, Tia, Tic, Tie}, KTI1 [NCBI Gene 100305855], Gy4 [NCBI Gene 547899], LOXB1 (lipoxygenase) [NCBI Gene 547836] {aka L-4, LOX1.5, LOX4, VSP94, lox1gm4}
- **Diseases:** hypertrophy (MESH:D006984), gastrointestinal discomfort (MESH:D005767), gastrointestinal problems (MESH:D012817), inflammatory (MESH:D007249), intestinal damage (MESH:D007410), hyperplasia (MESH:D006965), diarrhea (MESH:D003967), weight gain (MESH:D015430)
- **Chemicals:** Carbohydrates (MESH:D002241), oil (MESH:D009821), fatty acid (MESH:D005227), glycitein (MESH:C086566), daidzein (MESH:C004742), Carbon (MESH:D002244), phytosterols (MESH:D010840), tannins (MESH:D013634), triterpenoid (MESH:D014315), starch (MESH:D013213), isoflavones (MESH:D007529), isoleucine (MESH:D007532), Nitrogen (MESH:D009584), amino acid (MESH:D000596), vitamin E (MESH:D014810), glucose-6-phosphate (MESH:D019298), stachyose (MESH:C005695), Polysaccharides (MESH:D011134), disulfide (MESH:D004220), Zn (MESH:D015032), Phosphorus (MESH:D010758), oligosaccharides (MESH:D009844), potassium (MESH:D011188), Sugars (MESH:D000073893), acid (MESH:D000143), hexane (MESH:D006586), sulfur (MESH:D013455), IP6 (MESH:D010833), raffinose (MESH:D011887), fats (MESH:D005223), methionine (MESH:D008715), grain oil (-), Saponins (MESH:D012503), galactose (MESH:D005690), Ca (MESH:D002118), threonine (MESH:D013912), magnesium (MESH:D008274), myo-inositol (MESH:D007294), lecithin (MESH:D054709), glucose (MESH:D005947), aglycone (MESH:C458179), cellulose (MESH:D002482), tryptophan (MESH:D014364), SDS (MESH:D012967), essential amino acid (MESH:D000601), EMS (MESH:D005020), lysine (MESH:D008239), myo-inositol-3-phosphate (MESH:C052128), genistein (MESH:D019833), sucrose (MESH:D013395), Fe (MESH:D007501), cysteine (MESH:D003545), lipid (MESH:D008055), valine (MESH:D014633), phospholipid (MESH:D010743), beta-amyrin (MESH:C036380), daidzin (MESH:C013908), leucine (MESH:D007930), fructose (MESH:D005632)
- **Species:** Homo sapiens (human, species) [taxon 9606], Glycine max (soybean, species) [taxon 3847], Sus scrofa (pig, species) [taxon 9823], Glycine soja (wild soybean, species) [taxon 3848]

## Full text

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## Figures

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## References

164 references — full list in the complete paper: https://tomesphere.com/paper/PMC12957170/full.md

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Source: https://tomesphere.com/paper/PMC12957170