Rice Gene LC2 Keeps Leaves Flat by Suppressing Rolling-Cell Growth Program

Rice breeders have long prized a subtly curved leaf: moderately rolled blades make plants more erect and better able to withstand drought, but the molecular machinery that decides which way a leaf rolls has remained murky. A new study in BMC Plant Biology, based on CRISPR/Cas9-edited rice, now shows that the gene leaf inclination 2 (LC2) acts as a brake on leaf rolling, and that removing that brake triggers an outward, or abaxial, curl through a chain of effects reaching from chromatin marks to chlorogenic acid metabolism. The team, led by researchers working in the cultivar Nipponbare, introduced frameshift mutations into LC2 and examined the resulting leaves cell by cell.

The mutants rolled abaxially — the blade curled outward toward the underside — and showed a significantly increased leaf rolling index. The culprit, cytologically, was the bulliform layer: the lc2 mutants carried both more bulliform cells and larger ones than wild-type plants. Transcriptome sequencing pointed to a single conspicuous suspect.

Loss of LC2 function strongly upregulated OsZHD1, a gene whose overexpression alone is sufficient to induce abaxial leaf rolling in rice. The authors then showed how LC2 holds OsZHD1 in check through two mechanisms. First, LC2 maintains repressive H3K27me3 — a histone modification associated with silenced chromatin — across the whole OsZHD1 gene body.

Second, LC2 protein occupies putative strong enhancer elements located within the 3' untranslated region of OsZHD1, a region typically thought of as post-transcriptional territory but increasingly recognized as a landing zone for regulatory factors. When LC2 is knocked out, both brakes come off and OsZHD1 expression rises. The regulatory ripples did not stop there.

Two auxin transport genes, the efflux carrier genes OsPIN1b and OsPILS7a, were also considerably upregulated in the mutant, hinting that altered auxin distribution accompanies the change in leaf geometry, though the study stops short of demonstrating a causal role for auxin in the rolling phenotype. To connect cell shape to chemistry, the researchers integrated transcriptomic and metabolomic data from flag leaves at the booting stage. Core structural genes of the phenylpropanoid pathway — including OsPAL and OsPTAL — and of the flavonoid biosynthetic branch, among them OsCHS, OsCHI, OsF3'H, OsF3'H9 and CYP98A, were significantly upregulated in the lc2 mutant relative to wild type.

That transcriptional shift was matched at the metabolite level by a significant accumulation of caffeoylquinic acid, better known as chlorogenic acid, a key precursor channeled toward lignin synthesis. Because lignin deposition influences the mechanical properties of developing cell walls, the authors propose that this metabolic shift participates in bulliform cell development and is associated with the abaxial rolling seen in the mutant. The study is careful about the direction of causality.

The evidence establishes that LC2 loss upregulates OsZHD1, that OsZHD1 overexpression can itself drive abaxial rolling, and that phenylpropanoid and flavonoid gene expression and chlorogenic acid levels rise in parallel with the phenotype. Whether the metabolic changes are a driver of bulliform cell enlargement or a downstream consequence remains an open question, and the work was carried out in a single japonica cultivar background using an early-access, peer-reviewed version of the article that is still subject to editorial revision. Even with those caveats, the findings fill in an important piece of rice architecture biology.

Identifying LC2 as a negative regulator of OsZHD1 — acting through both histone modification and enhancer occupancy in an unexpected genomic neighborhood — gives breeders and genome editors a defined regulatory node to tune. It also suggests that leaf shape is not purely a hormone-and-cell-division story: specialized metabolism, traditionally studied in the context of stress and defense, appears woven into the morphogenesis of the leaf blade itself. For the field, the study reframes abaxial rolling not as a simple mechanical accident of oversized bulliform cells but as the output of a transcriptional and metabolic program that can be switched on by removing a single chromatin-associated brake.

Subject of Research: Molecular genetics of abaxial leaf rolling in rice mediated by LC2, OsZHD1 and phenylpropanoid metabolism

Article Title: Loss of leaf inclination 2 function leads to abaxial leaf rolling in rice due to upregulation of OsZHD1 and association with phenylpropanoid and flavonoid metabolism

Article References: Wang, Z., Zheng, K., Yang, D., Du, J., Sun, S., Zhang, Z., Lu, G.-H., & Guo, H. (2026). Loss of leaf inclination 2 function leads to abaxial leaf rolling in rice due to upregulation of OsZHD1 and association with phenylpropanoid and flavonoid metabolism. BMC Plant Biology. https://doi.org/10.1186/s12870-026-10291-5

Image Credits: AI Generated

DOI: 10.1186/s12870-026-10291-5

Keywords: rice, LC2, OsZHD1, leaf rolling, bulliform cells, CRISPR/Cas9, H3K27me3, phenylpropanoid, flavonoid, chlorogenic acid, auxin transport, plant architecture