Jing Xu

Cultivated soybean [ Glycine max (L.) Merr.], prized for its high protein and oil contents, was domesticated approximately 5000 years ago in the temperate regions of China. Today, soybean cultivation has expanded globally, including into suboptimal environments, particularly in low‐latitude regions such as Brazil, India and parts of Africa. This expansion aims to supply high‐quality protein feed for local livestock industries while addressing challenges of poverty and malnutrition. However, the greatest challenge for soybean adaptation in these regions lies in balancing environmental stresses—such as short‐day lengths, extreme temperatures, diseases and poor soil conditions—with the need to meet the world's growing demand for soybeans. Breeders have made significant strides in developing varieties adapted to short‐day conditions, unfavourable temperatures, severe diseases and harsh soil environments. Researchers are now delving deeper into the adaptation strategies of soybean in low‐latitude regions to uncover underlying mechanisms and guide next‐generation breeding efforts. Herein, we summarise the molecular mechanisms underlying soybean's response to low‐latitude environmental stresses. A comprehensive understanding of these mechanisms will provide critical insights for breeding widely adapted soybean varieties and further accelerate the global expansion of soybean cultivation in low‐latitude regions.

Faithful chromosome segregation is essential for both mitotic and meiotic cell division. The anaphase-promoting complex/cyclosome (APC/C) and its coactivators are required for meiotic chromosome segregation, but their potential targets and regulatory mechanisms remain unclear in plants. Here, we performed a ubiquitinome analysis and show that Arabidopsis thaliana Aurora 1 (AUR1) is over-ubiquitinated at lysine 102 in the coactivator Cell Division Cycle 20.1 (cdc20.1) mutants and that AUR1 overexpression can partially rescue the cdc20.1 meiotic defect. We also demonstrate that APC/C ubiquitinates AUR1, leading to its degradation through the 26S proteasome pathway. Moreover, the APC/C subunit and coactivators Cell Cycle Switch 52 A2/B (CCS52A2/B) and CDC20.1 interact with AUR1 both in vitro and in vivo. Intriguingly, CCS52A2/B promotes AUR1 ubiquitination and degradation, while CDC20.1 prevents AUR1 degradation. Consistent with this finding, AUR1 levels are lower in cdc20.1 and higher in ccs52 mutants relative to Col-0, and mutation of CCS52A2/B causes defects in meiotic spindle assembly and homologous chromosome segregation. Genetic analyses demonstrate that Arabidopsis anaphase-promoting complex/cyclosome subunit 8 (APC8), CDC20.1, CCS52 and AUR1 act in the same pathway to control meiotic spindle assembly and homologous chromosome segregation. Thus, this work provides mechanistic insight into the role of APC/C coactivators in regulating AUR1 homeostasis during meiosis in plants.