23 research outputs found
Involvement of Arabidopsis BIG protein in cell death mediated by Myo- Inositol homeostasis
International audienc
Balancing selection at a wing pattern locus is associated with major shifts in genome-wide patterns of diversity and gene flow
Polymorphism at a mimicry supergene maintained by opposing frequency-dependent selection pressures
International audienceExplaining the maintenance of adaptive diversity within populations is a long-standing goal in evolutionary biology, with important implications for conservation, medicine, and agriculture. Adaptation often leads to the fixation of beneficial alleles, and therefore it erodes local diversity so that understanding the coexistence of multiple adaptive phenotypes requires deciphering the ecological mechanisms that determine their respective benefits. Here, we show how antagonistic frequency-dependent selection (FDS), generated by natural and sexual selection acting on the same trait, maintains mimicry polymorphism in the toxic butterfly Heliconius numata. Positive FDS imposed by predators on mimetic signals favors the fixation of the most abundant and best-protected wing-pattern morph, thereby limiting polymor-phism. However, by using mate-choice experiments, we reveal disassortative mate preferences of the different wing-pattern morphs. The resulting negative FDS on wing-pattern alleles is consistent with the excess of heterozygote genotypes at the supergene locus controlling wing-pattern variation in natural populations of H. numata. The combined effect of positive and negative FDS on visual signals is sufficient to maintain a diversity of morphs displaying accurate mimicry with other local prey, although some of the forms only provide moderate protection against predators. Our findings help understand how alternative adaptive phenotypes can be maintained within populations and emphasize the need to investigate interactions between selective pressures in other cases of puzzling adaptive polymorphism. disassortative mating | selection conflicts | MĂŒllerian mimicry | aposematism | warning signal
Unravelling the genes forming the wing pattern supergene in the polymorphic butterfly Heliconius numata
Background Unravelling the genetic basis of polymorphic characters is central to our understanding of the origins and diversification of living organisms. Recently, supergenes have been implicated in a wide range of complex polymorphisms, from adaptive colouration in butterflies and fish to reproductive strategies in birds and plants. The concept of a supergene is now a hot topic in biology, and identification of its functional elements is needed to shed light on the evolution of highly divergent adaptive traits. Here, we apply different gene expression analyses to study the supergene P that controls polymorphism of mimetic wing colour patterns in the neotropical butterfly Heliconius numata. Results We performed de novo transcriptome assembly and differential expression analyses using high-throughput Illumina RNA sequencing on developing wing discs of different H. numata morphs. Within the P interval, 30 and 17 of the 191 transcripts were expressed differentially in prepupae and day-1 pupae, respectively. Among these is the gene cortex, known to play a role in wing pattern formation in Heliconius and other Lepidoptera. Our in situ hybridization experiments confirmed the relationship between cortex expression and adult wing patterns. Conclusions This study found the majority of genes in the P interval to be expressed in the developing wing discs during the critical stages of colour pattern formation, and detect drastic changes in expression patterns in multiple genes associated with structural variants. The patterns of expression of cortex only partially recapitulate the variation in adult phenotype, suggesting that the remaining phenotypic variation could be controlled by other genes within the P interval. Although functional studies on cortex are now needed to determine its exact developmental role, our results are in accordance with the classical supergene hypothesis, whereby several genes inherited together due to tight linkage control a major developmental switch
Selection of Valid Reference Genes for Reverse Transcription Quantitative PCR Analysis in Heliconius numata
Developmental Consequences of Defective ATG7-Mediated Autophagy in Humans
BACKGROUND
Autophagy is the major intracellular degradation route in mammalian cells. Systemic ablation of core autophagy-related (ATG) genes in mice leads to embryonic or perinatal lethality, and conditional models show neurodegeneration. Impaired autophagy has been associated with a range of complex human diseases, yet congenital autophagy disorders are rare.
METHODS
We performed a genetic, clinical, and neuroimaging analysis involving five families. Mechanistic investigations were conducted with the use of patient-derived fibroblasts, skeletal muscle-biopsy specimens, mouse embryonic fibroblasts, and yeast.
RESULTS
We found deleterious, recessive variants in human ATG7, a core autophagy-related gene encoding a protein that is indispensable to classical degradative autophagy. Twelve patients from five families with distinct ATG7 variants had complex neurodevelopmental disorders with brain, muscle, and endocrine involvement. Patients had abnormalities of the cerebellum and corpus callosum and various degrees of facial dysmorphism. These patients have survived with impaired autophagic flux arising from a diminishment or absence of ATG7 protein. Although autophagic sequestration was markedly reduced, evidence of basal autophagy was readily identified in fibroblasts and skeletal muscle with loss of ATG7. Complementation of different model systems by deleterious ATG7 variants resulted in poor or absent autophagic function as compared with the reintroduction of wild-type ATG7.
CONCLUSIONS
We identified several patients with a neurodevelopmental disorder who have survived with a severe loss or complete absence of ATG7, an essential effector enzyme for autophagy without a known functional paralogue. (Funded by the Wellcome Centre for Mitochondrial Research and others.)
Recommended from our members
Developmental Consequences of Defective ATG7-Mediated Autophagy in Humans
BACKGROUND
Autophagy is the major intracellular degradation route in mammalian cells. Systemic ablation of core autophagy-related (ATG) genes in mice leads to embryonic or perinatal lethality, and conditional models show neurodegeneration. Impaired autophagy has been associated with a range of complex human diseases, yet congenital autophagy disorders are rare.
METHODS
We performed a genetic, clinical, and neuroimaging analysis involving five families. Mechanistic investigations were conducted with the use of patient-derived fibroblasts, skeletal muscle-biopsy specimens, mouse embryonic fibroblasts, and yeast.
RESULTS
We found deleterious, recessive variants in human ATG7, a core autophagy-related gene encoding a protein that is indispensable to classical degradative autophagy. Twelve patients from five families with distinct ATG7 variants had complex neurodevelopmental disorders with brain, muscle, and endocrine involvement. Patients had abnormalities of the cerebellum and corpus callosum and various degrees of facial dysmorphism. These patients have survived with impaired autophagic flux arising from a diminishment or absence of ATG7 protein. Although autophagic sequestration was markedly reduced, evidence of basal autophagy was readily identified in fibroblasts and skeletal muscle with loss of ATG7. Complementation of different model systems by deleterious ATG7 variants resulted in poor or absent autophagic function as compared with the reintroduction of wild-type ATG7.
CONCLUSIONS
We identified several patients with a neurodevelopmental disorder who have survived with a severe loss or complete absence of ATG7, an essential effector enzyme for autophagy without a known functional paralogue. (Funded by the Wellcome Centre for Mitochondrial Research and others.)
Polymorphism at a mimicry supergene maintained by opposing frequency-dependent selection pressures
Convergence in light transmission properties of transparent wing areas in clearwing mimetic butterflies
MĂŒllerian mimicry is a positive interspecific interaction, whereby co-occurring defended prey species share a common aposematic signal that advertises their defences to predators. In Lepidoptera, aposematic species typically harbour conspicuous opaque wing colour pattern, which have convergent optical properties, as perceived by predators. Surprisingly, some aposematic mimetic species have partially or totally transparent wings, which raises the question of whether optical properties of such transparent areas are also under selection for convergence. To answer this question and to investigate how transparency is achieved in the first place, we conducted a comparative study of optics and structures of transparent wings in neotropical mimetic clearwing Lepidoptera. We quantified transparency by spectrophotometry and characterised clearwing microstructures and nanostructures by microscopy imaging. We show that transparency is convergent among co-mimics in the eyes of predators, despite a large diversity of underlying micro- and nanostructures. Notably, we reveal that nanostructure density largely influences light transmission. While transparency is primarily produced by modification of microstructure features, nanostructures may provide a way to fine-tune the degree of transparency. This study calls for a change of paradigm in transparent mimetic lepidoptera: transparency not only enables camouflage but can also be part of aposematic signals.MĂŒllerian mimicry is a positive interspecific interaction, whereby co-occurring defended prey species share a common aposematic signal that advertises their defences to predators. In Lepidoptera, aposematic species typically harbour conspicuous opaque wing colour pattern, which have convergent optical properties, as perceived by predators. Surprisingly, some aposematic mimetic species have partially or totally transparent wings, which raises the question of whether optical properties of such transparent areas are also under selection for convergence. To answer this question and to investigate how transparency is achieved in the first place, we conducted a comparative study of optics and structures of transparent wings in neotropical mimetic clearwing Lepidoptera. We quantified transparency by spectrophotometry and characterised clearwing microstructures and nanostructures by microscopy imaging. We show that transparency is convergent among co-mimics in the eyes of predators, despite a large diversity of underlying micro-and nanostructures. Notably, we reveal that nanostructure densit
Mimicry can drive convergence in structural and light transmission features of transparent wings in Lepidoptera
International audienceMĂŒllerian mimicry is a positive interspecific interaction, whereby co-occurring defended prey species share a common aposematic signal. In Lepidoptera, aposematic species typically harbour conspicuous opaque wing colour patterns with convergent optical properties among co-mimetic species. Surprisingly, some aposematic mimetic species have partially transparent wings, raising the questions of whether optical properties of transparent patches are also convergent, and of how transparency is achieved. Here, we conducted a comparative study of wing optics, micro and nanostructures in neotropical mimetic clearwing Lepidoptera, using spectrophotometry and microscopy imaging. We show that transparency, as perceived by predators, is convergent among co-mimics in some mimicry rings. Underlying micro- and nanostructures are also sometimes convergent despite a large structural diversity. We reveal that while transparency is primarily produced by microstructure modifications, nanostructures largely influence light transmission, potentially enabling additional fine-tuning in transmission properties. This study shows that transparency might not only enable camouflage but can also be part of aposematic signals