RESUMO
The innate immune system detects pathogens via germline-encoded receptors that bind to conserved pathogen ligands called pathogen-associated molecular patterns (PAMPs). Here we consider an additional strategy of pathogen sensing called effector-triggered immunity (ETI). ETI involves detection of pathogen-encoded virulence factors, also called effectors. Pathogens produce effectors to manipulate hosts to create a replicative niche and/or block host immunity. Unlike PAMPs, effectors are often diverse and rapidly evolving and can thus be unsuitable targets for direct detection by germline-encoded receptors. Effectors are instead often sensed indirectly via detection of their virulence activities. ETI is a viable strategy for pathogen sensing and is used across diverse phyla, including plants, but the molecular mechanisms of ETI are complex compared to simple receptor/ligand-based PAMP detection. Here we survey the mechanisms and functions of ETI, with a particular focus on emerging insights from animal studies. We suggest that many examples of ETI may remain to be discovered, hiding in plain sight throughout immunology.
Assuntos
Reconhecimento da Imunidade Inata , Moléculas com Motivos Associados a Patógenos , Humanos , Animais , Moléculas com Motivos Associados a Patógenos/metabolismo , VirulênciaRESUMO
Our understanding of the functions of the IL-1 superfamily cytokine and damage-associated molecular pattern IL-33 continues to evolve with our understanding of homeostasis and immunity. The early findings that IL-33 is a potent driver of type 2 immune responses promoting parasite expulsion, but also inflammatory diseases like allergy and asthma, have been further supported. Yet, as the importance of a type 2 response in tissue repair and homeostasis has emerged, so has the fundamental importance of IL-33 to these processes. In this review, we outline an evolving understanding of IL-33 immunobiology, paying particular attention to how IL-33 directs a network of ST2+ regulatory T cells, reparative and regulatory macrophages, and type 2 innate lymphoid cells that are fundamental to tissue development, homeostasis, and repair.
Assuntos
Hipersensibilidade , Interleucina-33 , Animais , Citocinas , Homeostase , Humanos , Imunidade Inata , LinfócitosRESUMO
In 1952, Alan Turing published the reaction-diffusion (RD) mathematical framework, laying the foundations of morphogenesis as a self-organized process emerging from physicochemical first principles. Regrettably, this approach has been widely doubted in the field of developmental biology. First, we summarize Turing's line of thoughts to alleviate the misconception that RD is an artificial mathematical construct. Second, we discuss why phenomenological RD models are particularly effective for understanding skin color patterning at the meso/macroscopic scales, without the need to parameterize the profusion of variables at lower scales. More specifically, we discuss how RD models (a) recapitulate the diversity of actual skin patterns, (b) capture the underlying dynamics of cellular interactions, (c) interact with tissue size and shape, (d) can lead to ordered sequential patterning, (e) generate cellular automaton dynamics in lizards and snakes, (f) predict actual patterns beyond their statistical features, and (g) are robust to model variations. Third, we discuss the utility of linear stability analysis and perform numerical simulations to demonstrate how deterministic RD emerges from the underlying chaotic microscopic agents.
Assuntos
Modelos Biológicos , Pigmentação da Pele , Animais , Morfogênese , Comunicação Celular , Vertebrados , Difusão , Padronização CorporalRESUMO
Patterns are ubiquitous in living systems and underlie the dynamic organization of cells, tissues, and embryos. Mathematical frameworks have been devised to account for the self-organization of biological patterns, most famously the Turing framework. Patterns can be defined in space, for example, to form stripes; in time, such as during oscillations; or both, to form traveling waves. The formation of these patterns can have different origins: purely chemical, purely mechanical, or a combination of the two. Beyond the variety of molecular implementations of such patterns, we emphasize the unitary principles associated with them, across scales in space and time, within a general mechanochemical framework. We illustrate where such mechanisms of pattern formation arise in biological systems from cellular to tissue scales, with an emphasis on morphogenesis. Our goal is to convey a picture of pattern formation that draws attention to the principles rather than solely to specific molecular mechanisms.
Assuntos
Modelos Biológicos , MorfogêneseRESUMO
Recognition of microbe-associated molecular patterns (MAMPs) is crucial for the plant's immune response. How this sophisticated perception system can be usefully deployed in roots, continuously exposed to microbes, remains a mystery. By analyzing MAMP receptor expression and response at cellular resolution in Arabidopsis, we observed that differentiated outer cell layers show low expression of pattern-recognition receptors (PRRs) and lack MAMP responsiveness. Yet, these cells can be gated to become responsive by neighbor cell damage. Laser ablation of small cell clusters strongly upregulates PRR expression in their vicinity, and elevated receptor expression is sufficient to induce responsiveness in non-responsive cells. Finally, localized damage also leads to immune responses to otherwise non-immunogenic, beneficial bacteria. Damage-gating is overridden by receptor overexpression, which antagonizes colonization. Our findings that cellular damage can "switch on" local immune responses helps to conceptualize how MAMP perception can be used despite the presence of microbial patterns in the soil.
Assuntos
Arabidopsis/imunologia , Doenças das Plantas/imunologia , Doenças das Plantas/microbiologia , Raízes de Plantas/imunologia , Receptores de Reconhecimento de Padrão/metabolismo , Arabidopsis/crescimento & desenvolvimento , Arabidopsis/microbiologia , Arabidopsis/efeitos da radiação , Proteínas de Arabidopsis/metabolismo , Proteínas de Arabidopsis/efeitos da radiação , Ascorbato Peroxidases/metabolismo , Ascorbato Peroxidases/efeitos da radiação , Flagelina/farmacologia , Regulação da Expressão Gênica de Plantas/efeitos dos fármacos , Regulação da Expressão Gênica de Plantas/efeitos da radiação , Terapia a Laser/métodos , Proteínas de Membrana/metabolismo , Proteínas de Membrana/efeitos da radiação , Microscopia Confocal , Raízes de Plantas/crescimento & desenvolvimento , Raízes de Plantas/microbiologia , Raízes de Plantas/efeitos da radiação , Proteínas Quinases/metabolismo , Proteínas Quinases/efeitos da radiação , Receptores de Reconhecimento de Padrão/efeitos da radiação , Transdução de Sinais/efeitos dos fármacos , Transdução de Sinais/efeitos da radiação , Imagem com Lapso de TempoRESUMO
There is an unmet clinical need for improved tissue and liquid biopsy tools for cancer detection. We investigated the proteomic profile of extracellular vesicles and particles (EVPs) in 426 human samples from tissue explants (TEs), plasma, and other bodily fluids. Among traditional exosome markers, CD9, HSPA8, ALIX, and HSP90AB1 represent pan-EVP markers, while ACTB, MSN, and RAP1B are novel pan-EVP markers. To confirm that EVPs are ideal diagnostic tools, we analyzed proteomes of TE- (n = 151) and plasma-derived (n = 120) EVPs. Comparison of TE EVPs identified proteins (e.g., VCAN, TNC, and THBS2) that distinguish tumors from normal tissues with 90% sensitivity/94% specificity. Machine-learning classification of plasma-derived EVP cargo, including immunoglobulins, revealed 95% sensitivity/90% specificity in detecting cancer. Finally, we defined a panel of tumor-type-specific EVP proteins in TEs and plasma, which can classify tumors of unknown primary origin. Thus, EVP proteins can serve as reliable biomarkers for cancer detection and determining cancer type.
Assuntos
Biomarcadores Tumorais/metabolismo , Vesículas Extracelulares/metabolismo , Neoplasias/diagnóstico , Animais , Biomarcadores Tumorais/sangue , Linhagem Celular , Proteínas de Choque Térmico HSC70/metabolismo , Humanos , Aprendizado de Máquina , Camundongos , Camundongos Endogâmicos C57BL , Proteínas dos Microfilamentos/metabolismo , Neoplasias/metabolismo , Proteoma/análise , Proteoma/metabolismo , Proteômica/métodos , Sensibilidade e Especificidade , Tetraspanina 29/metabolismo , Proteínas rap de Ligação ao GTP/metabolismoRESUMO
Distinguishing infectious pathogens from harmless microorganisms is essential for animal health. The mechanisms used to identify infectious microbes are not fully understood, particularly in metazoan hosts that eat bacteria as their food source. Here, we characterized a non-canonical pattern-recognition system in Caenorhabditis elegans (C. elegans) that assesses the relative threat of virulent Pseudomonas aeruginosa (P. aeruginosa) to activate innate immunity. We discovered that the innate immune response in C. elegans was triggered by phenazine-1-carboxamide (PCN), a toxic metabolite produced by pathogenic strains of P. aeruginosa. We identified the nuclear hormone receptor NHR-86/HNF4 as the PCN sensor in C. elegans and validated that PCN bound to the ligand-binding domain of NHR-86/HNF4. Activation of NHR-86/HNF4 by PCN directly engaged a transcriptional program in intestinal epithelial cells that protected against P. aeruginosa. Thus, a bacterial metabolite is a pattern of pathogenesis surveilled by nematodes to identify a pathogen in its bacterial diet.
Assuntos
Proteínas de Caenorhabditis elegans , Caenorhabditis elegans , Animais , Proteínas de Caenorhabditis elegans/genética , Proteínas de Caenorhabditis elegans/metabolismo , Regulação da Expressão Gênica , Receptores Citoplasmáticos e Nucleares/metabolismo , Imunidade Inata , Bactérias , Pseudomonas aeruginosa/metabolismoRESUMO
Vertebrates exhibit a wide range of color patterns, which play critical roles in mediating intra- and interspecific communication. Because of their diversity and visual accessibility, color patterns offer a unique and fascinating window into the processes underlying biological organization. In this review, we focus on describing many of the general principles governing the formation and evolution of color patterns in different vertebrate groups. We characterize the types of patterns, review the molecular and developmental mechanisms by which they originate, and discuss their role in constraining or facilitating evolutionary change. Lastly, we outline outstanding questions in the field and discuss different approaches that can be used to address them. Overall, we provide a unifying conceptual framework among vertebrate systems that may guide research into naturally evolved mechanisms underlying color pattern formation and evolution.
Assuntos
Evolução Biológica , Pigmentação , Animais , Pigmentação/genética , Vertebrados/genéticaRESUMO
Both the presence of an abnormal complement of chromosomes (aneuploidy) and an increased frequency of chromosome missegregation (chromosomal instability) are hallmarks of cancer. Analyses of cancer genome data have identified certain aneuploidy patterns in tumors; however, the bases behind their selection are largely unexplored. By establishing time-resolved long-term adaptation protocols, we found that human cells adapt to persistent spindle assembly checkpoint (SAC) inhibition by acquiring specific chromosome arm gains and losses. Independently adapted populations converge on complex karyotypes, which over time are refined to contain ever smaller chromosomal changes. Of note, the frequencies of chromosome arm gains in adapted cells correlate with those detected in cancers, suggesting that our cellular adaptation approach recapitulates selective traits that dictate the selection of aneuploidies frequently observed across many cancer types. We further engineered specific aneuploidies to determine the genetic basis behind the observed karyotype patterns. These experiments demonstrated that the adapted and engineered aneuploid cell lines limit CIN by extending mitotic duration. Heterozygous deletions of key SAC and APC/C genes recapitulated the rescue phenotypes of the monosomic chromosomes. We conclude that aneuploidy-induced gene dosage imbalances of individual mitotic regulators are sufficient for altering mitotic timing to reduce CIN.
Assuntos
Pontos de Checagem da Fase M do Ciclo Celular , Neoplasias , Humanos , Pontos de Checagem da Fase M do Ciclo Celular/genética , Aneuploidia , Neoplasias/genética , Instabilidade Cromossômica/genética , Cariótipo , Fuso Acromático/genética , MitoseRESUMO
Macrophages initiate inflammatory responses via the transcription factor NFκB. The temporal pattern of NFκB activity determines which genes are expressed and thus, the type of response that ensues. Here, we examined how information about the stimulus is encoded in the dynamics of NFκB activity. We generated an mVenus-RelA reporter mouse line to enable high-throughput live-cell analysis of primary macrophages responding to host- and pathogen-derived stimuli. An information-theoretic workflow identified six dynamical features-termed signaling codons-that convey stimulus information to the nucleus. In particular, oscillatory trajectories were a hallmark of responses to cytokine but not pathogen-derived stimuli. Single-cell imaging and RNA sequencing of macrophages from a mouse model of Sjögren's syndrome revealed inappropriate responses to stimuli, suggestive of confusion of two NFκB signaling codons. Thus, the dynamics of NFκB signaling classify immune threats through six signaling codons, and signal confusion based on defective codon deployment may underlie the etiology of some inflammatory diseases.
Assuntos
Códon/genética , Macrófagos/fisiologia , NF-kappa B/genética , Transdução de Sinais/genética , Animais , Células Cultivadas , Citocinas/genética , Modelos Animais de Doenças , Regulação da Expressão Gênica/genética , Inflamação/genética , Camundongos , Camundongos Endogâmicos C57BL , Síndrome de Sjogren/genética , Fator de Transcrição RelA/genéticaRESUMO
The number of cancer survivors continues to increase in the United States due to the growth and aging of the population as well as advances in early detection and treatment. To assist the public health community in better serving these individuals, the American Cancer Society and the National Cancer Institute collaborate triennially to estimate cancer prevalence in the United States using incidence and survival data from the Surveillance, Epidemiology, and End Results cancer registries, vital statistics from the Centers for Disease Control and Prevention's National Center for Health Statistics, and population projections from the US Census Bureau. Current treatment patterns based on information in the National Cancer Database are presented for the most prevalent cancer types by race, and cancer-related and treatment-related side-effects are also briefly described. More than 18 million Americans (8.3 million males and 9.7 million females) with a history of cancer were alive on January 1, 2022. The 3 most prevalent cancers are prostate (3,523,230), melanoma of the skin (760,640), and colon and rectum (726,450) among males and breast (4,055,770), uterine corpus (891,560), and thyroid (823,800) among females. More than one-half (53%) of survivors were diagnosed within the past 10 years, and two-thirds (67%) were aged 65 years or older. One of the largest racial disparities in treatment is for rectal cancer, for which 41% of Black patients with stage I disease receive proctectomy or proctocolectomy compared to 66% of White patients. Surgical receipt is also substantially lower among Black patients with non-small cell lung cancer, 49% for stages I-II and 16% for stage III versus 55% and 22% for White patients, respectively. These treatment disparities are exacerbated by the fact that Black patients continue to be less likely to be diagnosed with stage I disease than White patients for most cancers, with some of the largest disparities for female breast (53% vs 68%) and endometrial (59% vs 73%). Although there are a growing number of tools that can assist patients, caregivers, and clinicians in navigating the various phases of cancer survivorship, further evidence-based strategies and equitable access to available resources are needed to mitigate disparities for communities of color and optimize care for people with a history of cancer. CA Cancer J Clin. 2022;72:409-436.
Assuntos
Carcinoma Pulmonar de Células não Pequenas , Neoplasias Pulmonares , American Cancer Society , Feminino , Humanos , Masculino , National Cancer Institute (U.S.) , Sobrevivência , Estados Unidos/epidemiologiaRESUMO
The overall 5-year relative survival rate for all cancers combined is now 68%, and there are over 16.9 million survivors in the United States. Evidence from laboratory and observational studies suggests that factors such as diet, physical activity, and obesity may affect risk for recurrence and overall survival after a cancer diagnosis. The purpose of this American Cancer Society guideline is to provide evidence-based, cancer-specific recommendations for anthropometric parameters, physical activity, diet, and alcohol intake for reducing recurrence and cancer-specific and overall mortality. The audiences for this guideline are health care providers caring for cancer survivors as well as cancer survivors and their families. The guideline is intended to serve as a resource for informing American Cancer Society programs, health policy, and the media. Sources of evidence that form the basis of this guideline are systematic literature reviews, meta-analyses, pooled analyses of cohort studies, and large randomized clinical trials published since 2012. Recommendations for nutrition and physical activity during cancer treatment, informed by current practice, large cancer care organizations, and reviews of other expert bodies, are also presented. To provide additional context for the guidelines, the authors also include information on the relationship between health-related behaviors and comorbidities, long-term sequelae and patient-reported outcomes, and health disparities, with attention to enabling survivors' ability to adhere to recommendations. Approaches to meet survivors' needs are addressed as well as clinical care coordination and resources for nutrition and physical activity counseling after a cancer diagnosis.
Assuntos
Sobreviventes de Câncer , Neoplasias , American Cancer Society , Dieta , Exercício Físico , Humanos , Neoplasias/terapia , Sobreviventes , Estados Unidos/epidemiologiaRESUMO
Lytic cell death culminates in cell swelling and plasma membrane rupture (PMR). The cellular contents released, including proteins, metabolites, and nucleic acids, can act as danger signals and induce inflammation. During regulated cell death (RCD), lysis is actively initiated and can be preceded by an initial loss of membrane integrity caused by pore-forming proteins, allowing small molecules and cytokines to exit the cell. A recent seminal discovery showed that ninjurin1 (NINJ1) is the common executioner of PMR downstream of RCD, resulting in the release of large proinflammatory molecules and representing a novel target of cell death-associated lysis. We summarize recent developments in understanding membrane integrity and rupture of the plasma membrane with a focus on NINJ1.
Assuntos
Moléculas de Adesão Celular Neuronais , Membrana Celular , Humanos , Membrana Celular/metabolismo , Moléculas de Adesão Celular Neuronais/metabolismo , Animais , Fatores de Crescimento Neural/metabolismo , ApoptoseRESUMO
Cancer is a disease of aging and, as the world's population ages, the number of older persons with cancer is increasing and will make up a growing share of the oncology population in virtually every country. Despite this, older patients remain vastly underrepresented in research that sets the standards for cancer treatments. Consequently, most of what we know about cancer therapeutics is based on clinical trials conducted in younger, healthier patients, and effective strategies to improve clinical trial participation of older adults with cancer remain sparse. For this systematic review, the authors evaluated published studies regarding barriers to participation and interventions to improve participation of older adults in cancer trials. The quality of the available evidence was low and, despite a literature describing multifaceted barriers, only one intervention study aimed to increase enrollment of older adults in trials. The findings starkly amplify the paucity of evidence-based, effective strategies to improve participation of this underrepresented population in cancer trials. Within these limitations, the authors provide their opinion on how the current cancer research infrastructure must be modified to accommodate the needs of older patients. Several underused solutions are offered to expand clinical trials to include older adults with cancer. However, as currently constructed, these recommendations alone will not solve the evidence gap in geriatric oncology, and efforts are needed to meet older and frail adults where they are by expanding clinical trials designed specifically for this population and leveraging real-world data.
Assuntos
Geriatria/estatística & dados numéricos , Oncologia/estatística & dados numéricos , Neoplasias/terapia , Participação do Paciente/psicologia , Seleção de Pacientes , Idoso , Idoso de 80 Anos ou mais , Ensaios Clínicos como Assunto , Geriatria/métodos , Geriatria/tendências , Humanos , Oncologia/métodos , Oncologia/tendências , Neoplasias/diagnóstico , Participação do Paciente/estatística & dados numéricos , Estados UnidosRESUMO
Dendritic cells (DCs) are myeloid cells bridging the innate and adaptive immune system. By cross-presenting tumor-associated antigens (TAAs) liberated upon spontaneous or therapy-induced tumor cell death to T cells, DCs occupy a pivotal position in the cancer immunity cycle. Over the last decades, the mechanisms linking cancer cell death to DC maturation, have been the focus of intense research. Growing evidence supports the concept that the mere transfer of TAAs during the process of cell death is insufficient to drive immunogenic DC maturation unless this process is coupled with the release of immunomodulatory signals by dying cancer cells. Malignant cells succumbing to a regulated cell death variant called immunogenic cell death (ICD), foster a proficient interface with DCs, enabling their immunogenic maturation and engagement of adaptive immunity against cancer. This property relies on the ability of ICD to exhibit pathogen-mimicry hallmarks and orchestrate the emission of a spectrum of constitutively present or de novo-induced danger signals, collectively known as damage-associated molecular patterns (DAMPs). In this review, we discuss how DCs perceive and decode danger signals emanating from malignant cells undergoing ICD and provide an outlook of the major signaling and functional consequences of this interaction for DCs and antitumor immunity.
Assuntos
Morte Celular Imunogênica , Neoplasias , Humanos , Células Dendríticas , Morte Celular , Antígenos de Neoplasias , Imunidade AdaptativaRESUMO
Over the past decade our research has implemented a multimodal approach to human lymphopoiesis, combining clonal-scale mapping of lymphoid developmental architecture with the monitoring of dynamic changes in the pattern of lymphocyte generation across ontogeny. We propose that lymphopoiesis stems from founder populations of CD127/interleukin (IL)7R- or CD127/IL7R+ early lymphoid progenitors (ELPs) polarized respectively toward the T-natural killer (NK)/innate lymphoid cell (ILC) or B lineages, arising from newly characterized CD117lo multi-lymphoid progenitors (MLPs). Recent data on the lifelong lymphocyte dynamics of healthy donors suggest that, after birth, lymphopoiesis may become increasingly oriented toward the production of B lymphocytes. Stemming from this, we posit that there are three major developmental transitions, the first occurring during the neonatal period, the next at puberty, and the last during aging.
Assuntos
Envelhecimento , Linfopoese , Humanos , Envelhecimento/imunologia , Células Progenitoras Linfoides/citologia , Células Progenitoras Linfoides/metabolismo , Células Progenitoras Linfoides/imunologia , Linfócitos B/imunologia , Animais , Diferenciação Celular , Células Matadoras Naturais/imunologiaRESUMO
Although interferon-induced proteins with tetratricopeptide repeats (IFIT proteins) inhibit infection of many viruses by recognizing their RNA, the regulatory mechanisms involved remain unclear. Here we report a crystal structure of cap 0 (m7GpppN) RNA bound to human IFIT1 in complex with the C-terminal domain of human IFIT3. Structural, biochemical, and genetic studies suggest that IFIT3 binding to IFIT1 has dual regulatory functions: (1) extending the half-life of IFIT1 and thereby increasing its steady-state amounts in cells; and (2) allosterically regulating the IFIT1 RNA-binding channel, thereby enhancing the specificity of recognition for cap 0 but not cap 1 (m7GpppNm) or 5'-ppp RNA. Mouse Ifit3 lacks this key C-terminal domain and does not bind mouse Ifit1. The IFIT3 interaction with IFIT1 is important for restricting infection of viruses lacking 2'-O methylation in their RNA cap structures. Our experiments establish differences in the regulation of IFIT1 orthologs and define targets for modulation of human IFIT protein activity.
Assuntos
Proteínas de Transporte/metabolismo , Peptídeos e Proteínas de Sinalização Intracelular/metabolismo , Proteínas de Ligação a RNA/metabolismo , Proteínas Adaptadoras de Transdução de Sinal , Animais , Proteínas de Transporte/química , Proteínas de Transporte/genética , Regulação da Expressão Gênica , Interações Hospedeiro-Patógeno/genética , Humanos , Peptídeos e Proteínas de Sinalização Intracelular/química , Peptídeos e Proteínas de Sinalização Intracelular/genética , Metilação , Camundongos , Modelos Moleculares , Conformação Molecular , Ligação Proteica , Domínios e Motivos de Interação entre Proteínas , Estabilidade Proteica , RNA/química , RNA/genética , RNA/metabolismo , Proteínas de Ligação a RNA/química , Proteínas de Ligação a RNA/genética , Especificidade da Espécie , Relação Estrutura-AtividadeRESUMO
The American Cancer Society (ACS) publishes the Diet and Physical Activity Guideline to serve as a foundation for its communication, policy, and community strategies and, ultimately, to affect dietary and physical activity patterns among Americans. This guideline is developed by a national panel of experts in cancer research, prevention, epidemiology, public health, and policy, and reflects the most current scientific evidence related to dietary and activity patterns and cancer risk. The ACS guideline focuses on recommendations for individual choices regarding diet and physical activity patterns, but those choices occur within a community context that either facilitates or creates barriers to healthy behaviors. Therefore, this committee presents recommendations for community action to accompany the 4 recommendations for individual choices to reduce cancer risk. These recommendations for community action recognize that a supportive social and physical environment is indispensable if individuals at all levels of society are to have genuine opportunities to choose healthy behaviors. This 2020 ACS guideline is consistent with guidelines from the American Heart Association and the American Diabetes Association for the prevention of coronary heart disease and diabetes as well as for general health promotion, as defined by the 2015 to 2020 Dietary Guidelines for Americans and the 2018 Physical Activity Guidelines for Americans.
Assuntos
Exercício Físico/fisiologia , Comportamento Alimentar/fisiologia , Promoção da Saúde/normas , Estilo de Vida Saudável/fisiologia , Neoplasias/prevenção & controle , American Cancer Society , Humanos , Estados UnidosRESUMO
Self-organized spatial patterns are a common feature of complex systems, ranging from microbial communities to mussel beds and drylands. While the theoretical implications of these patterns for ecosystem-level processes, such as functioning and resilience, have been extensively studied, empirical evidence remains scarce. To address this gap, we analyzed global drylands along an aridity gradient using remote sensing, field data, and modeling. We found that the spatial structure of the vegetation strengthens as aridity increases, which is associated with the maintenance of a high level of soil multifunctionality, even as aridity levels rise up to a certain threshold. The combination of these results with those of two individual-based models indicate that self-organized vegetation patterns not only form in response to stressful environmental conditions but also provide drylands with the ability to adapt to changing conditions while maintaining their functioning, an adaptive capacity which is lost in degraded ecosystems. Self-organization thereby plays a vital role in enhancing the resilience of drylands. Overall, our findings contribute to a deeper understanding of the relationship between spatial vegetation patterns and dryland resilience. They also represent a significant step forward in the development of indicators for ecosystem resilience, which are critical tools for managing and preserving these valuable ecosystems in a warmer and more arid world.
Assuntos
Microbiota , Resiliência Psicológica , Ecossistema , SoloRESUMO
Languages disfavor word forms containing sequences of similar or identical consonants, due to the biomechanical and cognitive difficulties posed by patterns of this sort. However, the specific evolutionary processes responsible for this phenomenon are not fully understood. Words containing sequences of identical consonants may be more likely to arise than those without; processes of word form mutation may be more likely to remove than create sequences of identical consonants in word forms; finally, words containing identical consonants may die out more frequently than those without. Phylogenetic analyses of the evolution of homologous word forms indicate that words with identical consonants arise less frequently than those without. However, words with identical consonants do not die out more frequently than those without. Further analyses reveal that forms with identical consonants are replaced in basic meaning functions more frequently than words without. Taken together, results suggest that the underrepresentation of sequences of identical consonants is overwhelmingly a by-product of constraints on word form coinage, though processes related to word usage also serve to ensure that such patterns are infrequent in more salient vocabulary items. These findings clarify aspects of processes of lexical evolution and competition that take place during language change, optimizing communicative systems.