With the rapid emergence and distribution of red crown rot (RCR) across countries, durable sources of resistance against Calonectria ilicicola in soybean [Glycine max (L.) Merrill] is required to control the disease. We employed two RIL populations for the experiment. We identified 15 and 14 QTLs associated with RCR resistance in ZM6 and MN populations, respectively, totaling 29 QTLs. Six and eight QTLs had phenotypic variation above 10% in ZM6 and MN populations, respectively. We identified six (6) “QTL hotspots” for resistance to RCR from the ZM6 and MN RIL populations on chromosomes 1, 7, 10, 11, 13, and 18. Gene annotations, gene ontology enhancement, and RNA sequencing assessment detected 23 genes located within six “QTL Hotspots” as potential candidate genes that could govern RCR resistance in soybeans. Our data will generally assist breeders in rapidly and effectively incorporating RCR resistance into high-yielding accession through marker-assisted selection.

Photosynthetic efficiency decreases as light energy surpasses the photosynthesis capacity. This study was designed to investigate the potential effects of high-intensity light on the photooxidation-prone mutant 812HS of rice and its wild-type 812S during yellow and recovering stages. Results showed that in the yellowing stage, light oxidation occurs due to the exposure of mutant 812HS leaves to the high sunlight, which causes yellowing of the leaves, leading to a reduction in the photochemical activities, physiological mechanisms, and protein contents in mutant 812HS. In the recovery stage, mutant 812HS leaves were exposed to the maximum high brightness, the mutant’s leaves were draped with a dark cover to decrease the exposure of leaves of the plants from direct sunlight, which leads to the restoration of the green color again to the mutant 812HS leaves, leading to improving the performance of the photochemical activities, physiological mechanisms, and protein contents in mutant 812HS. Exposing leaves of mutant 812HS to high light at the yellow stage also resulted in a decrease in the net photosynthetic rate (Pn) in carotenoids content and chlorophyll a and b. Similarly, chlorophyll fluorescence of mutant 812HS decreased in (O-I-J-I-P) curves, and the ATP content, Mg²⁺-ATPase, and Ca²⁺-ATPase activities also decreased. An increase in energy dissipation was observed, while ABS/RC, DI0/RC, and TR0/RC values in mutant 812HS at the yellow stage increased. During photooxidation, an increase in O₂^•– and H₂O₂ contents was observed in mutant 812HS. While O₂^•– and H₂O₂ contents were decreased in mutant 812HS at the recovery stage. The rate of thylakoid membrane protein content was significantly decreased in mutant 812HS at the yellow stage, while at the recovery stage, there was no significant decrease. Our findings showed that photooxidation prompted oxidative damages and lipid peroxidation that caused severe damages to the membranes of the cell, photosynthetic pigments degradation, protein levels, and photosynthesis inhibition in mutant 812HS.

Drought and salinity are two major factors limiting soybean productivity worldwide, and both stresses can negatively affect plant growth in similar manners by disrupting cellular redox homeostasis and metabolism. However, the regulatory networks coordinating transcriptional control and metabolic adaptation under both types of stress remain poorly understood. Here, we demonstrate that the R2R3–MYB transcription factors GmMYB60a and GmMYB60b serve as core negative regulators of drought and salt tolerance in soybean. Loss‐of‐function mutations in GmMYB60a/b clearly increased stress tolerance, which was associated with reduced reactive oxygen species accumulation and increased antioxidant capacity. The GmMYB60 proteins directly bind to and transcriptionally repress GmCYS20 , a key gene involved in cysteine biosynthesis, thereby reducing cellular cysteine and glutathione pools. Notably, the GmCYS20 protein physically interacts with GmMYB60 in the nucleus and weakens its ability to bind DNA, resulting in the formation of a transcription–metabolic feedback loop that stabilizes redox homeostasis under stress. Furthermore, the stress‐responsive NAC transcription factor GmNAC3 directly suppresses GmMYB60 expression, thereby linking environmental signals to metabolic regulation. Together, these findings reveal a hierarchical GmNAC3–GmMYB60–GmCYS20 regulatory module that coordinates cysteine homeostasis and oxidative stress responses by integrating transcriptional repression with metabolic feedback. This work provides mechanistic insights into soybean stress adaptation and identifies promising genetic targets for improving soybean resistance to drought and salinity.