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SUMMARY : Nuclear restorer of fertility (Rf) genes suppress the effects of mitochondrial genes causing cytoplasmic male sterility (CMS), a condition in which plants fail to produce viable pollen. Rf genes, many of which encode RNA‐binding pentatricopeptide repeat (PPR) proteins, are applied in hybrid breeding to overcome CMS used to block self‐pollination of the seed parent. Here, we characterise the repertoire of restorer‐of‐fertility‐like (RFL) PPR genes in barley (Hordeum vulgare). We found 26 RFL genes in the reference genome ('Morex') and an additional 51 putative orthogroups (POGs) in a re‐sequencing data set from 262 barley genotypes and landraces. Whereas the sequences of some POGs are highly conserved across hundreds of barley accessions, the sequences of others are much more variable. High sequence variation strongly correlates with genomic location – the most variable genes are found in a cluster on chromosome 1H. A much higher likelihood of diversifying selection was found for genes within this cluster than for genes present as singlets. This work includes a comprehensive analysis of the patterns of intraspecific variation of RFL genes. The RFL sequences characterised in this study will be useful for the development of new markers for fertility restoration loci. Significance statement: Restorer of fertility genes are applied in plant breeding to overcome mitochondrially conditioned male sterility in hybrid crop production. Although these genes are known to vary between related species, intraspecific variation in the gene family has not been comprehensively studied. By systematic analysis of restorer of fertility‐like sequences across hundreds of barley accessions, we show that a huge diversity of these RNA‐binding proteins exists within a single species, with strong diversifying selection on the residues known to determine binding specificity. [ABSTRACT FROM AUTHOR]

We produced 15 dissection lines of common wheat carrying segments of chromosome 1R of wild rye (Secale montanum) (1Rm) by the gametocidal system. Using the 1Rm dissection lines and previously established 24 dissection lines of chromosome 1R from cultivated rye (Secale cereale cv. 'Imperial') (1Ri), we conducted cytological mapping of 97 markers that were amplified in the 1Ri addition line. Sixty-eight of the 97 markers were amplified in the 1Rm addition line. To reveal what structural differentiation occurred in chromosome 1R during domestication, we compared the cytological map of chromosome 1Ri with that of chromosome 1Rm, and also with the previously published cytological map of chromosome 1R from wheat cultivar 'Burgas 2' (1RB). There was one discrepancy in marker order in the satellite region between chromosomes 1Ri and 1RB, while there were four discrepancies in marker order between chromosomes 1Ri and 1Rm. These results suggested that during the domestication of rye, some intrachromosomal rearrangements had occurred in chromosome 1R, although this chromosome is regarded as the most stable chromosome in the rye genome. [ABSTRACT FROM AUTHOR]

Free amino acids (FAAs) are key components of the global nitrogen cycle and important disinfection byproduct (DBP) precursors. The knowledge gap of FAA occurrence in source and engineered water is discussed in this paper. Solid phase extraction and post column derivatization was combined with gas chromatography–mass spectrometry to simultaneously detect μg/L concentrations of FAAs. This method efficiently detects alanine (Ala), threonine (Thr), serine (Ser), valine (Val), leucine (Leu), isoleucine (Ile), proline (Pro), aspartic (Asp), phenylalanine (Phe), and glutamic acid (Glu) with good linearity, accuracy, and precision. An investigation of FAAs in surface waters in Zhejiang Province found concentrations of 1.48–14.73 μg/L Ala, 0.20–2.39 μg/L Thr, 0.41–7.84 μg/L Val, 0.21–6.86 μg/L Ser, 0.11–4.16 μg/L Leu, 0.57–1.54 μg/L Ile, 0.24–8.06 μg/L Pro, 0.42–4.73 μg/L Asp, 0.30–3.01 μg/L Phe, and 0.12–3.83 μg/L Glu. Phe and tyrosine (Tyr) exhibited higher trichloromethane (TCM) formation (1029–1148 μg/mmolAA) than dichloroacetonitrile (DCAN) formation (333–347 μg/mmolAA). Asp and Glu demonstrated the opposite trend: higher DCAN (570–1106 μg/mmolAA) formation than TCM (137–506 μg/mmolAA). [ABSTRACT FROM AUTHOR]

Idiopathic pulmonary fibrosis (IPF) is a devastating condition characterized by progressive lung scarring and uncontrolled fibroblast proliferation, inevitably leading to organ dysfunction and mortality. Although elevated iron levels have been observed in patients and animal models of lung fibrosis, the mechanisms linking iron dysregulation to lung fibrosis pathogenesis, particularly the role of macrophages in orchestrating this process, remain poorly elucidated. Here we evaluate iron metabolism in macrophages during pulmonary fibrosis using both in vivo and in vitro approaches. In murine bleomycin- and amiodarone-induced pulmonary fibrosis models, we observed significant iron deposition and lipid peroxidation in pulmonary macrophages. Intriguingly, the ferroptosis regulator glutathione peroxidase 4 (GPX4) was upregulated in pulmonary macrophages following bleomycin instillation, a finding corroborated by single-cell RNA sequencing analysis. Moreover, macrophages isolated from fibrotic mouse lungs exhibited increased transforming growth factor (TGF)-β1 expression that correlated with lipid peroxidation. In vitro, iron overload in bone marrow-derived macrophages triggered lipid peroxidation and TGF-β1 upregulation, which was effectively suppressed by ferroptosis inhibitors. When cocultured with iron-overloaded macrophages, lung fibroblasts exhibited heightened activation, evidenced by increased α-smooth muscle actin and fibronectin expression. Importantly, this profibrotic effect was attenuated by treating macrophages with a ferroptosis inhibitor or blocking TGF-β receptor signaling in fibroblasts. Collectively, our study elucidates a novel mechanistic paradigm in which the accumulation of iron within macrophages initiates lipid peroxidation, thereby amplifying TGF-β1 production, subsequently instigating fibroblast activation through paracrine signaling. Thus, inhibiting iron overload and lipid peroxidation warrants further exploration as a strategy to suppress fibrotic stimulation by disease-associated macrophages. NEW & NOTEWORTHY This study investigates the role of iron in pulmonary fibrosis, specifically focusing on macrophage-mediated mechanisms. Iron accumulation in fibrotic lung macrophages triggers lipid peroxidation and an upregulation of transforming growth factor (TGF)-β1 expression. Coculturing iron-laden macrophages activates lung fibroblasts in a TGF-β1-dependent manner, which can be mitigated by ferroptosis inhibitors. These findings underscore the potential of targeting iron overload and lipid peroxidation as a promising strategy to alleviate fibrotic stimulation provoked by disease-associated macrophages.

Background: Hepatic steatosis is a significant pathological feature of fatty liver disease (FLD) which is widely spread with no effective treatment available. Previous studies suggest that chromium (Cr) intake reduces lipid deposition in the liver in animals. However, the connection between blood Cr and hepatic steatosis among humans remains inconclusive., Methods: Using the data from the National Health and Nutrition Examination Survey (NHANES) 2017-2020, we performed a cross-sectional analysis, including 4,926 participants. The controlled attenuation parameter (CAP) measured by the vibration controlled transient elastography (VCTE) was used to evaluate the degree of liver steatosis. Weighted univariate regression, multivariate linear regression, smooth fitting curves and subgroup analysis were used. In addition, we carried out trend tests, multiple interpolations, and interaction analyses to conduct sensitivity analyses., Results: After adjusting with various covariables, multivariate linear regression analysis demonstrated a significant negative correlation between blood Cr and CAP [β (95% CI) = -5.62 (-11.02, -0.21)]. The negative correlation between blood Cr and CAP was more significant in the males, 50-59 years, overweight, hypercholesterolemia, HDL-C ≥ 65 mg/dL, HbA1c (5.70-6.10 %), HOMA-IR (0.12-2.76), total bilirubin (0.30-0.40 mg/dL), ever alcohol consumption subjects. Of note, the relationships between blood Cr and CAP followed a U-shaped curve in the smokers and non-smokers, with blood Cr thresholds of 0.48, 0.69 μg/L, respectively., Conclusions: There is an independently negative correlation between blood Cr and hepatic steatosis in American. Our study provides clinical researchers with a new insight into the prospective prevention of hepatic steatosis., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Xiang, Zhou, Wang, Xue, Cao, Shen, Zhu, Xu, Zhou and Shang.)