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The Cold War was not only about the imperial ambitions of the super powers, their military strategies, and antagonistic ideologies. It was also about conflicting worldviews and their correlates in the daily life of the societies involved. The term \"Cold War Culture\" is often used in a broad sense to describe media influences, social practices, and symbolic representations as they shape, and are shaped by, international relations. Yet, it remains in question whether - or to what extent - the Cold War Culture model can be applied to European societies, both in the East and the West. While every European country had to adapt to the constraints imposed by the Cold War, individual development was affected by specific conditions as detailed in these chapters. This volume offers an important contribution to the international debate on this issue of the Cold War impact on everyday life by providing a better understanding of its history and legacy in Eastern and Western Europe.

• The plant hormone jasmonic acid (JA) is involved in the cold stress response, and the inducer of CBF expression 1 (ICE1)- C-repeat binding factor (CBF) regulatory cascade plays a key role in the regulation of cold stress tolerance. In this study, we showed that a novel B-box (BBX) protein MdBBX37 positively regulates JA-mediated cold-stress resistance in apple. • We found that MdBBX37 bound to the MdCBF1 and MdCBF4 promoters to activate their transcription, and also interacted with MdICE1 to enhance the transcriptional activity of MdICE1 on MdCBF1, thus promoting its cold tolerance. • Two JA signaling repressors, MdJAZ1 and MdJAZ2 (JAZ, JAZMONATE ZIM-DOMAIN), interacted with MdBBX37 to repress the transcriptional activity of MdBBX37 on MdCBF1 and MdCBF4, and also interfered with the interaction between MdBBX37 and MdICE1, thus negatively regulating JA-mediated cold tolerance. E3 ligase MdMIEL1 (MIEL1, MYB30-Interacting E3 Ligase1) reduced MdBBX37-improved cold resistance by mediating ubiquitination and degradation of the MdBBX37 protein. • The data reveal that MIEL1 and JAZ proteins co-regulate JA-mediated cold stress tolerance through the BBX37-ICE1-CBF module in apple. These results will aid further examination of the post-translational modification of BBX proteins and the regulatory mechanism of JA-mediated cold stress tolerance.

Background Daye No.3 is a novel cultivar of alfalfa ( Medicago sativa L.) that is well suited for cultivation in high-altitude regions such as the Qinghai‒Tibet Plateau owing to its high yield and notable cold resistance. However, the limited availability of transcriptomic information has hindered our investigation into the potential mechanisms of cold tolerance in this cultivar. Consequently, we conducted de novo transcriptome assembly to overcome this limitation. Subsequently, we compared the patterns of gene expression in Daye No. 3 during cold acclimatization and exposure to cold stress at various time points. Results A total of 15 alfalfa samples were included in the transcriptome assembly, resulting in 141.97 Gb of clean bases. A total of 441 DEGs were induced by cold acclimation, while 4525, 5016, and 8056 DEGs were identified at 12 h, 24 h, and 36 h after prolonged cold stress at 4 °C, respectively. The consistency between the RT‒qPCR and transcriptome data confirmed the accuracy and reliability of the transcriptomic data. KEGG enrichment analysis revealed that many genes related to photosynthesis were enriched under cold stress. STEM analysis demonstrated that genes involved in nitrogen metabolism and the TCA cycle were consistently upregulated under cold stress, while genes associated with photosynthesis, particularly antenna protein genes, were downregulated. PPI network analysis revealed that ubiquitination-related ribosomal proteins act as hub genes in response to cold stress. Additionally, the plant hormone signaling pathway was activated under cold stress, suggesting its vital role in the cold stress response of alfalfa. Conclusions Ubiquitination-related ribosomal proteins induced by cold acclimation play a crucial role in early cold signal transduction. As hub genes, these ubiquitination-related ribosomal proteins regulate a multitude of downstream genes in response to cold stress. The upregulation of genes related to nitrogen metabolism and the TCA cycle and the activation of the plant hormone signaling pathway contribute to the enhanced cold tolerance of alfalfa.

Evergreen conifers are champions of winter survival, based on their remarkable ability to acclimate to cold and develop cold hardiness. Counterintuitively, autumn cold acclimation is triggered not only by exposure to low temperature, but also by a combination of decreasing temperature, decreasing photoperiod and changes in light quality. These environmental cues control a network of signaling pathways that coordinate cold acclimation and cold hardiness in overwintering conifers, leading to cessation of growth, bud dormancy, freezing tolerance and changes in energy metabolism. Advances in genomic, transcriptomic and metabolomic tools for conifers have improved our understanding of how trees sense and respond to changes in temperature and light during cold acclimation and the development of cold hardiness, but there remain considerable gaps deserving further research in conifers. In the first section of this review, we focus on the physiological mechanisms used by evergreen conifers to adjust metabolism seasonally and to protect overwintering tissues against winter stresses. In the second section, we review how perception of low temperature and photoperiod regulate the induction of cold acclimation. Finally, we explore the evolutionary context of cold acclimation in conifers and evaluate challenges imposed on them by changing climate and discuss emerging areas of research in the field.

Summary Cold stress significantly affects the growth and productivity of tomatoes. Despite the known involvement of jasmonate (JA) in cold stress responses, the underlying mechanism remains to be elucidated. Here, we observed that JA peaked 24 h after cold treatment. The expression of the SlLOXD gene, a key player in JA biosynthesis, also peaked at 24 h of cold exposure, and mutation in SlLOXD reduced JA content and cold tolerance. Downstream of JA signalling, the transcription factor SlMYC2 was implicated in enhancing cold resistance by directly binding to the SlCBF1/2 promoters. Furthermore, the SlMYC2‐silenced plants and mutants exhibited increased sensitivity to cold damage. Additionally, SlMYB15 directly bound to the SlLOXD and SlMYC2 promoters. Within 6 h of cold stress, SlMYB15 activated SlLOXD expression while repressing SlMYC2 expression. Between 6 and 24 h, the expression level of SlMYB15 decreased, thereby alleviating the repression of SlMYC2 expression. SlMYC2 further enhanced JA signalling through the transcriptional activation of SlLOXD, thus improving cold tolerance in tomato plants. These findings provide valuable insights into the dynamic regulation of the SlLOXD–SlMYC2 –CBF1/2 module by SlMYB15 and its critical role in tomato cold stress responses.

Apple (Malus × domestica) trees are vulnerable to freezing temperatures. However, there has been only limited success in developing cold-hardy cultivars. This lack of progress is due at least partly to lack of understanding of the molecular mechanisms of freezing tolerance in apple. In this study, we evaluated the potential roles for two R2R3 MYB transcription factors (TFs), MYB88 and the paralogous FLP (MYB124), in cold stress in apple and Arabidopsis. We found that MYB88 and MYB124 positively regulate freezing tolerance and cold-responsive gene expression in both apple and Arabidopsis. Chromatin-Immunoprecipitation-qPCR and electrophoretic mobility shift assays showed that MdMYB88/MdMYB124 act as direct regulators of the COLD SHOCK DOMAIN PROTEIN 3 (MdCSP3) and CIRCADIAN CLOCK ASSOCIATED 1 (MdCCA1) genes. Dual luciferase reporter assay indicated that MdCCA1 but not MdCSP3 activated the expression of MdCBF3 under cold stress. Moreover, MdMYB88 and MdMYB124 promoted anthocyanin accumulation and H2O2 detoxification in response to cold. Taken together, our results suggest that MdMYB88 and MdMYB124 positively regulate cold hardiness and cold-responsive gene expression under cold stress by C-REPEAT BINDING FACTOR (CBF)-dependent and CBF-independent pathways.

Cold stress is a major environmental factor that seriously affects plant growth and development, and influences crop productivity. Plants have evolved a series of mechanisms that allow them to adapt to cold stress at both the physiological and molecular levels. Over the past two decades, much progress has been made in identifying crucial components involved in cold-stress tolerance and dissecting their regulatory mechanisms. In this review, we summarize recent major advances in our understanding of cold signalling and put forward open questions in the field of plant cold-stress responses. Answering these questions should help elucidate the molecular mechanisms underlying plant tolerance to cold stress.

Introduction: Freezing cold injuries (FCI) are a common risk in extreme cold weather operations. Although the risks have long been recognised, injury occurrences tend to be sparse and geographically distributed, with relatively few cases to study in a systematic way. The first challenge to improve FCI medical management is to develop a common nomenclature for FCI classification. This is critical for the development of meaningful epidemiological reports on the magnitude and severity of FCI, for the standardisation of patient inclusion criteria for treatment studies, and for the development of clinical diagnosis and treatment algorithms. Methodology: A scoping review of the literature using PubMed and cross-checked with Google Scholar, using search terms related to freezing cold injury and frostbite, highlighted a paucity of published clinical papers and little agreement on classification schemes. Results: A total of 74 papers were identified, and 28 were included in the review. Published reports and studies can be generally grouped into four different classification schemes that are based on (1) injury morphology; (2) signs and symptoms; (3) pathophysiology; and (4) clinical outcome. The nomenclature in the different classification systems is not coherent and the discrete classification limits are not evidence based. Conclusions: All the classification systems are necessary and relevant to FCI medical management for sustainment of soldier health and performance in cold weather operations and winter warfare. Future FCI reports should clearly characterise the nature of the FCI into existing classification schemes for surveillance (morphology, symptoms, and appearance), identifying risk-factors, clinical guidelines, and agreed inclusion/exclusion criteria for a future treatment trial.