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Abstract Ferroptosis is a type of cell regulated necrosis triggered by intracellular phospholipid peroxidation, which is more immunogenic than apoptosis. Therefore, genes controlling ferroptosis may be promising candidate biomarkers for tumor therapy. In this study, we investigate the function of genes associated with ferroptosis in breast cancer (BC) and systematically evaluate the relationship between ferroptosis-related gene expression and prognosis of BC patients from the Cancer Genome Atlas database. By using the consensus clustering method, 1203 breast cancer samples were clustered into two clearly divided subgroups based on the expression of 237 ferroptosis-related genes. Then differentially expressed analysis and least absolute shrinkage and selection operator were used to identify the prognosis-related genes. Furthermore, the genetic risk signature was constructed using the expression of prognosis-related genes. Our results showed that the genetic risk signature can identify patient subgroups with distinct prognosis in either training cohort or validation, and the genetic risk signature was associated with the tumor immune microenvironment. Finally, the Cox regression analysis indicated that our risk signature was an independent prognostic factor for BC patients and this signature was verified by the polymerase chain reaction and western blot. Within this study, we identified a novel prognostic classifier based on five ferroptosis-related genes which may provide a new reference for the treatment of BRCA patients.

Abstract The main symptom of boron (B) deficiency in cotton is the formation of brown rings on leaf petioles. The objective of the present study was to determine the changes in the anatomical structure and chemical composition of petioles and photosynthesis of leaves in cotton under B deficiency. Compared to the control, B deficiency treatment resulted in large increases in the number of petioles with brown rings per plant (160.0%) and the number of rings on the petiole per functional leaf (711.1%) in cotton seedlings. The relative absorbance intensity in the fingerprint region of polysaccharide structure was decreased in petiole rings under B deficiency, while lignin contents were increased. Cotton plants mitigated the impairment of transport function in cotton petioles by increasing the areas of vascular bundles, phloem, xylem, and phloem fiber. Moreover, the stomatal conductance, photosynthetic rate, and transpiration rate in leaves were significantly decreased under B deficiency, thus impeding photosynthesis in cotton plants. Therefore, B deficiency reduces transport function in petioles and photosynthesis in leaves, and leads to the formation of noticeable brown rings on petioles of cotton seedlings.

Abstract An isobaric tags for relative and absolute quantitative (iTRAQ)-based quantitative proteomic approach was used to screen the differentially expressed proteins during control treatment (CK), aluminum (Al) and Al+ indole-3-acetic acid (IAA) treatment of wheat lines ET8 (Al-tolerant). Further, the the expression levels of auxin response factor (ARF), Aux/IAA, Mitogen activated protein kinase (MAPK) 2c, and MAPK1a were analyzed. Results showed that 16 proteins were determined to be differentially expressed in response to Al and IAA co-treatment compared with Al alone. Among them, MAPK2c and MAPK1a proteins displayed markedly differential expression during the processes. The expression of ARF2 was upregulated and Aux/IAA was downregulated by Al, while both in concentration- and time-dependent manners. Western-blot detection of MAPK2c and MAPK1a indicated that Al upregulated MAPK2c and downregulated MAPK1a in both concentration- and time-dependent manners. Exogenous IAA could promote the expression of MAPK2c, but inhibit the expression of MAPK1a in the presence/absence of Al. These findings indicated that IAA acted as one of the key signaling molecule controls the response mechanism of wheat malic acid efflux to Al stress through the suppression/activation of Aux/IAA and ARFs, and the activity of MAPK2c and MAPK1a were positively or negatively regulated.