Catalogue Search | MBRL
Are you sure you want to remove the book from the shelf?
{{itemTitle}}
12,993
result(s) for
"mimicry"
Sort by:
Plants in disguise : features of creatures in flowers and foliage
When you wander a woodland forest, skip through a sunlit meadow, or ramble down a dusty path, you might see a furry tail, a bristly beard, or a fuzzy toe. Did you catch a glimpse of an animal? Or was it a plant in disguise? These wild plants aren't wearing masks or funny noses, but each one displays a feature of a creature.
Book
Cheats and deceits : how animals and plants exploit and mislead
\"Stevens describes the remarkable range of ... adaptations in nature, and considers how they have evolved and increasingly been perfected as part of an arms race between predator and prey or host and parasite. He explores both classic and recent research of naturalists and biologists, showing how scientists find ways of testing the impact of particular behaviours and colourings on the animals it is meant to fool. Drawing on a wide range of examples, Stevens considers what deception tells us about the process of evolution and adaptation\"--Amazon.com.
Book
Mimicry between adult rove beetles and assassin bug nymphs with unequal defenses: antagonistic or mutualistic?
Defensive mimicry encompasses a continuum ranging from Batesian to Müllerian mimicry. Batesian mimicry involves antagonistic interactions between undefended and defended species, whereas Müllerian mimicry represents mutualistic interactions between species with comparable levels of defense. When mimicry occurs between species with unequal defensive abilities, it is termed quasi-Batesian mimicry, though whether such interactions are antagonistic or mutualistic remains debated. Despite their common occurrence in nature, few quasi-Batesian mimicry systems have been experimentally studied. Here, we investigated the mimetic interaction between two chemically defended insect species, the rove beetle Paederus fuscipes Curtis, 1826 (Coleoptera: Staphylinidae) and the assassin bug Sirthenea flavipes (Stål, 1855) (Hemiptera: Reduviidae), through behavioral assays with their potential predator, the pond frog Pelophylax nigromaculatus (Hallowell, 1861) (Anura: Ranidae), which naturally co-occurs with these insects in Japan. Adult P . fuscipes resemble S . flavipes nymphs in their conspicuous reddish-orange and black coloration. Under laboratory conditions, 45.8% of pond frogs rejected P . fuscipes adults, whereas 70.8% rejected S . flavipes nymphs, suggesting that the assassin bug nymphs are better defended. Prior exposure to S. flavipes increased frog rejection of P. fuscipes , whereas exposure to P. fuscipes slightly reduced rejection of S. flavipes . These results indicate that adult P . fuscipes may gain protective benefits from mimicry of S . flavipes nymphs, while the latter may incur a small cost.
Journal Article
Hidden wildlife : how animals hide in plain sight
\"Animals know that in order to survive, they must stay hidden--and, fortunately, nature helps them by providing coloration that camouflages them in their habitat ... [this book features] a wide variety of mammals, birds, insects, and sea creatures, and also offers kids advice on becoming better at spying animals out in the wild\"-- Provided by publisher.
Book
Mimicry in motion and morphology: do information limitation, trade-offs or compensation relax selection for mimetic accuracy?
Many animals mimic dangerous or undesirable prey as a defence from predators. We would expect predators to reliably avoid animals that closely resemble dangerous prey, yet imperfect mimics are common across a wide taxonomic range. There have been many hypotheses suggested to explain imperfect mimicry, but comparative tests across multiple mimicry systems are needed to determine which are applicable, and which—if any—represent general principles governing imperfect mimicry. We tested four hypotheses on Australian ant mimics and found support for only one of them: the information limitation hypothesis. A predator with incomplete information will be unable to discriminate some poor mimics from their models. We further present a simple model to show that predators are likely to operate with incomplete information because they forage and make decisions while they are learning, so might never learn to properly discriminate poor mimics from their models. We found no evidence that one accurate mimetic trait can compensate for, or constrain, another, or that rapid movement reduces selection pressure for good mimicry. We argue that information limitation may be a general principle behind imperfect mimicry of complex traits, while interactions between components of mimicry are unlikely to provide a general explanation for imperfect mimicry.
Journal Article
Reaction of Human Monoclonal Antibodies to SARS-CoV-2 Proteins With Tissue Antigens: Implications for Autoimmune Diseases
We sought to determine whether immune reactivity occurs between anti-SARS-CoV-2 protein antibodies and human tissue antigens, and whether molecular mimicry between COVID-19 viral proteins and human tissues could be the cause. We applied both human monoclonal anti-SARS-Cov-2 antibodies (spike protein, nucleoprotein) and rabbit polyclonal anti-SARS-Cov-2 antibodies (envelope protein, membrane protein) to 55 different tissue antigens. We found that SARS-CoV-2 antibodies had reactions with 28 out of 55 tissue antigens, representing a diversity of tissue groups that included barrier proteins, gastrointestinal, thyroid and neural tissues, and more. We also did selective epitope mapping using BLAST and showed similarities and homology between spike, nucleoprotein, and many other SARS-CoV-2 proteins with the human tissue antigens mitochondria M2, F-actin and TPO. This extensive immune cross-reactivity between SARS-CoV-2 antibodies and different antigen groups may play a role in the multi-system disease process of COVID-19, influence the severity of the disease, precipitate the onset of autoimmunity in susceptible subgroups, and potentially exacerbate autoimmunity in subjects that have pre-existing autoimmune diseases. Very recently, human monoclonal antibodies were approved for use on patients with COVID-19. The human monoclonal antibodies used in this study are almost identical with these approved antibodies. Thus, our results can establish the potential risk for autoimmunity and multi-system disorders with COVID-19 that may come from cross-reactivity between our own human tissues and this dreaded virus, and thus ensure that the badly-needed vaccines and treatments being developed for it are truly safe to use against this disease.
Journal Article
Epigenetic therapy induces transcription of inverted SINEs and ADAR1 dependency
Cancer therapies that target epigenetic repressors can mediate their effects by activating retroelements within the human genome. Retroelement transcripts can form double-stranded RNA (dsRNA) that activates the MDA5 pattern recognition receptor
1
–
6
. This state of viral mimicry leads to loss of cancer cell fitness and stimulates innate and adaptive immune responses
7
,
8
. However, the clinical efficacy of epigenetic therapies has been limited. To find targets that would synergize with the viral mimicry response, we sought to identify the immunogenic retroelements that are activated by epigenetic therapies. Here we show that intronic and intergenic SINE elements, specifically inverted-repeat Alus, are the major source of drug-induced immunogenic dsRNA. These inverted-repeat Alus are frequently located downstream of ‘orphan’ CpG islands
9
. In mammals, the ADAR1 enzyme targets and destabilizes inverted-repeat Alu dsRNA
10
, which prevents activation of the MDA5 receptor
11
. We found that ADAR1 establishes a negative-feedback loop, restricting the viral mimicry response to epigenetic therapy. Depletion of ADAR1 in patient-derived cancer cells potentiates the efficacy of epigenetic therapy, restraining tumour growth and reducing cancer initiation. Therefore, epigenetic therapies trigger viral mimicry by inducing a subset of inverted-repeats Alus, leading to an ADAR1 dependency. Our findings suggest that combining epigenetic therapies with ADAR1 inhibitors represents a promising strategy for cancer treatment.
Inverted-repeat Alu elements are the main source of drug-induced immunogenic double-stranded RNAs, which are destabilized by the RNA deaminase ADAR1, thereby limiting activation of the immune response.
Journal Article