Endoreduplication—repeated nuclear DNA replication without mitosis—is widespread in plants and correlates with cell expansion. Because enlarging cells must remodel their primary cell wall, the question arises of how these two processes are coordinated to set final cell size. In a study published in Nature Communications, Dr. Lei Li’s group at Peking University Institute of Advanced Agricultural Sciences / Shandong Laboratory of Advanced Agriculture Sciences in Weifang / State Key Laboratory of Wheat Improvement now provides the answer, showing that targeted degradation of cell-wall pectin licenses endocycle progression and pavement-cell growth.

 

 

TEOSINTE BRANCHED 1 / CYCLOIDEA / PCF (TCP) transcription factors are plant-specific regulators of cell growth and organ architecture. Among them, the eight CIN-TCP members (TCP2, 3, 4, 5, 10, 13, 17 and 24) are known cell-cycle modulators. Using the tcpΔ7 heptuple mutant, the authors observed dramatically smaller leaf pavement cells whose nuclei stalled at 8C and rarely progressed to 16C or higher (Fig. 1), indicating a block in endoreduplication.

 

Fig. 1. CIN-TCPs promote both cell expansion and endocycle progression.

 

Cell-wall chemistry revealed a marked accumulation of pectin in tcpΔ7. Transcriptome profiling identified POLYGALACTURONASE1 (PGL1), a pectin-degrading enzyme, as a direct transcriptional target of CIN-TCPs. Over-expressing PGL1 in tcpΔ7 (tcpΔ7 PGL1-OX) rescued cell expansion and restored the 8C → 16C transition, demonstrating that CIN-TCPs, via PGL1-mediated pectin degradation, relieve a physical constraint on the endocycle (Fig. 2).

 

Fig. 2. PGL1 complements the endocycle defect of tcpΔ7 and promotes leaf enlargement.

 

To corroborate this model, the authors exploited their previous finding that miR775 negatively regulates pectin synthesis. MIR775 overexpression, which lowers pectin levels, phenocopied the CIN-TCP/PGL1 effect, enhancing both cell size and the 8C → 16C transition (Fig. 3). Thus, two independent genetic circuits converge on pectin abundance to tune endocycle progression.

Fig. 3. Working model for pectin-mediated control of the endocycle.

 

By integrating these results with earlier work on the HY5–miR775–GALT9 pathway that governs organ size (Zhang et al., Plant Cell 2021) and hypocotyl growth during dark-to-light transitions (Zhang et al., Curr. Biol. 2025), the Li team now proposes a unified framework that links nuclear endocycle control, cell expansion and cell-wall remodelling. Their findings add a new node to the endocycle regulatory network and bridge two traditionally separate fields — cell-cycle control and cell-wall dynamics — offering a fresh theoretical scaffold for plant developmental biology.

 

Dr. Feng Shen (former PhD student, School of Life Sciences, Peking University) and Dr. He Zhang (postdoc, Peking University Modern Agriculture Research Institute) are co-first authors. Dr. He Zhang and Dr. Lei Li are co-corresponding authors. Additional contributors include Dr. Miaomiao Wan, Dr. Liang Xiao (visiting postdocs), Yanzhi Yang (PKU-MAL), Zheng Kuang (Beijing Academy of Agriculture and Forestry Sciences), and Prof. Genji Qin (School of Life Sciences, Peking University). Technical support was provided by Dr. Guilan Li and Jun Hu (National Center for Protein Sciences) and Guoqiang Wang (Xiao-E Biotech). The work was funded by the National Natural Science Foundation of China and the Taishan Scholar Program.

 

Paper link: https://doi.org/10.1038/s41467-025-59336-7