Convergent changes in gene expression associated with repeated transitions between hummingbird and bee pollinated flowers

AbstractThe repeated evolution of convergent floral shapes and colors in angiosperms has been largely interpreted as the response to pollinator-mediated selection to maximize attraction and efficiency of specific groups of pollinators. The genetic mechanisms contributing to certain flower traits have been studied in detail for model system species, but the extent by which flowers are free to vary and how predictable are the genetic changes underlying flower adaptation to pollinator shifts still remain largely unknown.Here, we aimed at detecting the genetic basis of the repeated evolution of flower phenotypes associated with pollinator shifts. We assembled and compared de novo transcriptomes of three phylogenetic independent pairs of Gesneriaceae species, each with contrasting flower phenotype adapted to either bee or hummingbird pollination. We assembled and analyzed a total of 14,059 genes and we showed that changes in expression in 550 of them was associated with the pollination syndromes. Among those, we observed genes with function linked to floral color, scent, shape and symmetry, as well as nectar composition. These genes represent candidates genes involved in the build-up of the convergent floral phenotypes.This study provides the first insights into the molecular mechanisms underlying the repeated evolution of pollination syndromes. Although the presence of additional lineage-specific responses cannot be excluded, these results suggest that the convergent evolution of genes expression is involved in the convergent build-up of the pollination syndromes. Future studies aiming to directly manipulate certain genes will integrate our knowledge on the key genes for floral transitions and the pace of floral evolution.Data availabilityRaw Illumina reads will be available in the Sequence Read Archive (SRA) in NCBI database. The assembled transcriptomes and their annotation will by available in DRYAD repository. Details and accession ID will be provided at the time of the manuscript acceptance.

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Chemical Basis of Floral Color Signals in Gesneriaceae: The Effect of Alternative Anthocyanin Pathways

Frontiers in Plant Science ◽

10.3389/fpls.2020.604389 ◽

2020 ◽

Vol 11 ◽

Author(s):

Ezgi Ogutcen ◽

Karine Durand ◽

Marina Wolowski ◽

Laura Clavijo ◽

Catherine Graham ◽

...

Keyword(s):

High Performance ◽

Flower Color ◽

Pollination Syndromes ◽

Angiosperm Evolution ◽

Ecological Diversification ◽

Floral Color ◽

Wide Range ◽

Hummingbird Pollination ◽

Color Signals ◽

Physical And Chemical

Changes in floral pigmentation can have dramatic effects on angiosperm evolution by making flowers either attractive or inconspicuous to different pollinator groups. Flower color largely depends on the type and abundance of pigments produced in the petals, but it is still unclear whether similar color signals rely on same biosynthetic pathways and to which extent the activation of certain pathways influences the course of floral color evolution. To address these questions, we investigated the physical and chemical aspects of floral color in the Neotropical Gesnerioideae (ca. 1,200 spp.), in which two types of anthocyanins, hydroxyanthocyanins, and deoxyanthocyanins, have been recorded as floral pigments. Using spectrophotometry, we measured flower reflectance for over 150 species representing different clades and pollination syndromes. We analyzed these reflectance data to estimate how the Gesnerioideae flowers are perceived by bees and hummingbirds using the visual system models of these pollinators. Floral anthocyanins were further identified using high performance liquid chromatography coupled to mass spectrometry. We found that orange/red floral colors in Gesnerioideae are produced either by deoxyanthocyanins (e.g., apigenidin, luteolinidin) or hydroxyanthocyanins (e.g., pelargonidin). The presence of deoxyanthocyanins in several lineages suggests that the activation of the deoxyanthocyanin pathway has evolved multiple times in the Gesnerioideae. The hydroxyanthocyanin-producing flowers span a wide range of colors, which enables them to be discriminated by hummingbirds or bees. By contrast, color diversity among the deoxyanthocyanin-producing species is lower and mainly represented at longer wavelengths, which is in line with the hue discrimination optima for hummingbirds. These results indicate that Gesnerioideae have evolved two different biochemical mechanisms to generate orange/red flowers, which is associated with hummingbird pollination. Our findings also suggest that the activation of the deoxyanthocyanin pathway has restricted flower color diversification to orange/red hues, supporting the potential constraining role of this alternative biosynthetic pathway on the evolutionary outcome of phenotypical and ecological diversification.

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Genetic architecture of floral traits in bee- and hummingbird-pollinated sister species of Aquilegia (columbine)

10.1101/2021.04.12.439277 ◽

2021 ◽

Author(s):

Molly B. Edwards ◽

Gary P. T. Choi ◽

Nathan J. Derieg ◽

Ya Min ◽

Angie C. Diana ◽

...

Keyword(s):

Qtl Mapping ◽

Candidate Genes ◽

Genetic Architecture ◽

Genetic Basis ◽

Single Locus ◽

Floral Traits ◽

Pollination Syndromes ◽

Evolutionary Consequence ◽

Floral Color ◽

Hummingbird Pollination

Interactions with animal pollinators have helped shape the stunning diversity of flower morphologies across the angiosperms. A common evolutionary consequence of these interactions is that some flowers have converged on suites of traits, or pollination syndromes, that attract and reward specific pollinator groups. Determining the genetic basis of these floral pollination syndromes can help us understand the processes that contributed to the diversification of the angiosperms. Here, we characterize the genetic architecture of a bee-to-hummingbird pollination shift in Aquilegia (columbine) using QTL mapping of 17 floral traits encompassing color, nectar composition, and organ morphology. In this system, we find that the genetic architectures underlying differences in floral color are quite complex, and we identify several likely candidate genes involved in anthocyanin and carotenoid floral pigmentation. Most morphological and nectar traits also have complex genetic underpinnings; however, one of the key floral morphological phenotypes, nectar spur curvature, is shaped by a single locus of large effect.

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Molecular Mechanisms of Complement System Proteins and Matrix Metalloproteinases in the Pathogenesis of Age-Related Macular Degeneration

Current Molecular Medicine ◽

10.2174/1566524019666190828150625 ◽

2019 ◽

Vol 19 (10) ◽

pp. 705-718 ◽

Cited By ~ 4

Author(s):

Naima Mansoor ◽

Fazli Wahid ◽

Maleeha Azam ◽

Khadim Shah ◽

Anneke I. den Hollander ◽

...

Keyword(s):

Matrix Metalloproteinases ◽

Macular Degeneration ◽

Complement System ◽

Molecular Mechanisms ◽

Critical Role ◽

Age Related Macular Degeneration ◽

Genetic Changes ◽

Complement System Proteins ◽

Age Related ◽

Common Genetic Variants

: Age-related macular degeneration (AMD) is an eye disorder affecting predominantly the older people above the age of 50 years in which the macular region of the retina deteriorates, resulting in the loss of central vision. The key factors associated with the pathogenesis of AMD are age, smoking, dietary, and genetic risk factors. There are few associated and plausible genes involved in AMD pathogenesis. Common genetic variants (with a minor allele frequency of >5% in the population) near the complement genes explain 40–60% of the heritability of AMD. The complement system is a group of proteins that work together to destroy foreign invaders, trigger inflammation, and remove debris from cells and tissues. Genetic changes in and around several complement system genes, including the CFH, contribute to the formation of drusen and progression of AMD. Similarly, Matrix metalloproteinases (MMPs) that are normally involved in tissue remodeling also play a critical role in the pathogenesis of AMD. MMPs are involved in the degradation of cell debris and lipid deposits beneath retina but with age their functions get affected and result in the drusen formation, succeeding to macular degeneration. In this review, AMD pathology, existing knowledge about the normal and pathological role of complement system proteins and MMPs in the eye is reviewed. The scattered data of complement system proteins, MMPs, drusenogenesis, and lipofusogenesis have been gathered and discussed in detail. This might add new dimensions to the understanding of molecular mechanisms of AMD pathophysiology and might help in finding new therapeutic options for AMD.

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HP1 drives de novo 3D genome reorganization in early Drosophila embryos

Nature ◽

10.1038/s41586-021-03460-z ◽

2021 ◽

Author(s):

Fides Zenk ◽

Yinxiu Zhan ◽

Pavel Kos ◽

Eva Löser ◽

Nazerke Atinbayeva ◽

...

Keyword(s):

Genome Organization ◽

Molecular Mechanisms ◽

High Throughput Sequencing ◽

De Novo ◽

Early Embryo ◽

Heterochromatin Protein ◽

Chromosome Conformation ◽

3D Genome ◽

Genome Reorganization

AbstractFundamental features of 3D genome organization are established de novo in the early embryo, including clustering of pericentromeric regions, the folding of chromosome arms and the segregation of chromosomes into active (A-) and inactive (B-) compartments. However, the molecular mechanisms that drive de novo organization remain unknown1,2. Here, by combining chromosome conformation capture (Hi-C), chromatin immunoprecipitation with high-throughput sequencing (ChIP–seq), 3D DNA fluorescence in situ hybridization (3D DNA FISH) and polymer simulations, we show that heterochromatin protein 1a (HP1a) is essential for de novo 3D genome organization during Drosophila early development. The binding of HP1a at pericentromeric heterochromatin is required to establish clustering of pericentromeric regions. Moreover, HP1a binding within chromosome arms is responsible for overall chromosome folding and has an important role in the formation of B-compartment regions. However, depletion of HP1a does not affect the A-compartment, which suggests that a different molecular mechanism segregates active chromosome regions. Our work identifies HP1a as an epigenetic regulator that is involved in establishing the global structure of the genome in the early embryo.

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Copy number-dependent DNA methylation of the Pyricularia oryzae MAGGY retrotransposon is triggered by DNA damage

Communications Biology ◽

10.1038/s42003-021-01836-5 ◽

2021 ◽

Vol 4 (1) ◽

Author(s):

Ba Van Vu ◽

Quyet Nguyen ◽

Yuki Kondo-Takeoka ◽

Toshiki Murata ◽

Naoki Kadotani ◽

...

Keyword(s):

Dna Methylation ◽

Copy Number ◽

Rna Silencing ◽

Molecular Mechanisms ◽

De Novo ◽

Pyricularia Oryzae ◽

Transcriptional Gene Silencing ◽

Physical Interaction ◽

Uncharacterized Protein ◽

Form Complex

AbstractTransposable elements are common targets for transcriptional and post-transcriptional gene silencing in eukaryotic genomes. However, the molecular mechanisms responsible for sensing such repeated sequences in the genome remain largely unknown. Here, we show that machinery of homologous recombination (HR) and RNA silencing play cooperative roles in copy number-dependent de novo DNA methylation of the retrotransposon MAGGY in the fungusPyricularia oryzae. Genetic and physical interaction studies revealed thatRecAdomain-containing proteins, includingP. oryzaehomologs ofRad51, Rad55, andRad57, together with an uncharacterized protein, Ddnm1, form complex(es) and mediate either the overall level or the copy number-dependence of de novo MAGGY DNA methylation, likely in conjunction with DNA repair. Interestingly,P. oryzaemutants of specific RNA silencing components (MoDCL1andMoAGO2)were impaired in copy number-dependence of MAGGY methylation. Co-immunoprecipitation of MoAGO2 and HR components suggested a physical interaction between the HR and RNA silencing machinery in the process.

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The Prion-Like Spreading of Alpha-Synuclein in Parkinson’s Disease: Update on Models and Hypotheses

International Journal of Molecular Sciences ◽

10.3390/ijms22158338 ◽

2021 ◽

Vol 22 (15) ◽

pp. 8338

Author(s):

Asad Jan ◽

Nádia Pereira Gonçalves ◽

Christian Bjerggaard Vaegter ◽

Poul Henning Jensen ◽

Nelson Ferreira

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Molecular Mechanisms ◽

De Novo ◽

Alpha Synuclein ◽

Experimental Models ◽

Cellular Factors ◽

Recent Developments ◽

Novel Targets ◽

Presynaptic Protein

The pathological aggregation of the presynaptic protein α-synuclein (α-syn) and propagation through synaptically coupled neuroanatomical tracts is increasingly thought to underlie the pathophysiological progression of Parkinson’s disease (PD) and related synucleinopathies. Although the precise molecular mechanisms responsible for the spreading of pathological α-syn accumulation in the CNS are not fully understood, growing evidence suggests that de novo α-syn misfolding and/or neuronal internalization of aggregated α-syn facilitates conformational templating of endogenous α-syn monomers in a mechanism reminiscent of prions. A refined understanding of the biochemical and cellular factors mediating the pathological neuron-to-neuron propagation of misfolded α-syn will potentially elucidate the etiology of PD and unravel novel targets for therapeutic intervention. Here, we discuss recent developments on the hypothesis regarding trans-synaptic propagation of α-syn pathology in the context of neuronal vulnerability and highlight the potential utility of novel experimental models of synucleinopathies.

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Examination of the Transcriptional Response to LaMIR166a Overexpression in Larix kaempferi (Lamb.) Carr

Biology ◽

10.3390/biology10070576 ◽

2021 ◽

Vol 10 (7) ◽

pp. 576

Author(s):

Yanru Fan ◽

Wanfeng Li ◽

Zhexin Li ◽

Shaofei Dang ◽

Suying Han ◽

...

Keyword(s):

Cell Lines ◽

Molecular Mechanisms ◽

Target Genes ◽

De Novo ◽

Pearson Correlation ◽

Transcriptional Response ◽

Correlation Coefficients ◽

Embryonic Cell ◽

Larix Kaempferi ◽

Transgenic Cell

The study of somatic embryogenesis can provide insight into early plant development. We previously obtained LaMIR166a-overexpressing embryonic cell lines of Larix kaempferi (Lamb.) Carr. To further elucidate the molecular mechanisms associated with miR166 in this species, the transcriptional profiles of wild-type (WT) and three LaMIR166a-overexpressing transgenic cell lines were subjected to RNA sequencing using the Illumina NovaSeq 6000 system. In total, 203,256 unigenes were generated using Trinity de novo assembly, and 2467 differentially expressed genes were obtained by comparing transgenic and WT lines. In addition, we analyzed the cleaved degree of LaMIR166a target genes LaHDZ31–34 in different transgenic cell lines by detecting the expression pattern of LaHdZ31–34, and their cleaved degree in transgenic cell lines was higher than that in WT. The downstream genes of LaHDZ31–34 were identified using Pearson correlation coefficients. Yeast one-hybrid and dual-luciferase report assays revealed that the transcription factors LaHDZ31–34 could bind to the promoters of LaPAP, LaPP1, LaZFP5, and LaPHO1. This is the first report of gene expression changes caused by LaMIR166a overexpression in Japanese larch. These findings lay a foundation for future studies on the regulatory mechanism of miR166.

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RNA-Seq reveals divergent gene expression between larvae with contrasting trophic modes in the poecilogonous polychaete Boccardia wellingtonensis

Scientific Reports ◽

10.1038/s41598-021-94646-y ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Álvaro Figueroa ◽

Antonio Brante ◽

Leyla Cárdenas

Keyword(s):

De Novo ◽

Juvenile Stage ◽

Type I ◽

Rna Seq ◽

Mrna Synthesis ◽

De Novo Transcriptome ◽

Larval Stages ◽

Divergent Gene ◽

Genetic Mechanisms ◽

Planktotrophic Larvae

AbstractThe polychaete Boccardia wellingtonensis is a poecilogonous species that produces different larval types. Females may lay Type I capsules, in which only planktotrophic larvae are present, or Type III capsules that contain planktotrophic and adelphophagic larvae as well as nurse eggs. While planktotrophic larvae do not feed during encapsulation, adelphophagic larvae develop by feeding on nurse eggs and on other larvae inside the capsules and hatch at the juvenile stage. Previous works have not found differences in the morphology between the two larval types; thus, the factors explaining contrasting feeding abilities in larvae of this species are still unknown. In this paper, we use a transcriptomic approach to study the cellular and genetic mechanisms underlying the different larval trophic modes of B. wellingtonensis. By using approximately 624 million high-quality reads, we assemble the de novo transcriptome with 133,314 contigs, coding 32,390 putative proteins. We identify 5221 genes that are up-regulated in larval stages compared to their expression in adult individuals. The genetic expression profile differed between larval trophic modes, with genes involved in lipid metabolism and chaetogenesis over expressed in planktotrophic larvae. In contrast, up-regulated genes in adelphophagic larvae were associated with DNA replication and mRNA synthesis.

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Comparative Transcriptome Analysis Reveals Genetic Mechanisms of Sugarcane Aphid Resistance in Grain Sorghum

International Journal of Molecular Sciences ◽

10.3390/ijms22137129 ◽

2021 ◽

Vol 22 (13) ◽

pp. 7129

Author(s):

Desalegn D. Serba ◽

Xiaoxi Meng ◽

James Schnable ◽

Elfadil Bashir ◽

J. P. Michaud ◽

...

Keyword(s):

Differential Expression ◽

Molecular Mechanisms ◽

Grain Sorghum ◽

Lipid Binding ◽

Multiple Time ◽

Melanaphis Sacchari ◽

Resistant Genotype ◽

Sugarcane Aphid ◽

Genetic Mechanisms ◽

Moderately Resistant

The sugarcane aphid, Melanaphis sacchari (Zehntner) (Hemiptera: Aphididae) (SCA), has become a major pest of grain sorghum since its appearance in the USA. Several grain sorghum parental lines are moderately resistant to the SCA. However, the molecular and genetic mechanisms underlying this resistance are poorly understood, which has constrained breeding for improved resistance. RNA-Seq was used to conduct transcriptomics analysis on a moderately resistant genotype (TAM428) and a susceptible genotype (Tx2737) to elucidate the molecular mechanisms underlying resistance. Differential expression analysis revealed differences in transcriptomic profile between the two genotypes at multiple time points after infestation by SCA. Six gene clusters had differential expression during SCA infestation. Gene ontology enrichment and cluster analysis of genes differentially expressed after SCA infestation revealed consistent upregulation of genes controlling protein and lipid binding, cellular catabolic processes, transcription initiation, and autophagy in the resistant genotype. Genes regulating responses to external stimuli and stress, cell communication, and transferase activities, were all upregulated in later stages of infestation. On the other hand, expression of genes controlling cell cycle and nuclear division were reduced after SCA infestation in the resistant genotype. These results indicate that different classes of genes, including stress response genes and transcription factors, are responsible for countering the physiological effects of SCA infestation in resistant sorghum plants.

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CACNA1A Mutation Linking Hemiplegic Migraine and Alternating Hemiplegia of Childhood

Cephalalgia ◽

10.1111/j.1468-2982.2008.01596.x ◽

2008 ◽

Vol 28 (8) ◽

pp. 887-891 ◽

Cited By ~ 34

Author(s):

B de Vries ◽

AH Stam ◽

F Beker ◽

AMJM van den Maagdenberg ◽

KRJ Vanmolkot ◽

...

Keyword(s):

Clinical Features ◽

Molecular Mechanisms ◽

De Novo ◽

Monozygotic Twin ◽

Familial Hemiplegic Migraine ◽

Hemiplegic Migraine ◽

Mutation Scanning ◽

Alternating Hemiplegia Of Childhood ◽

Neurological Phenotype ◽

Cacna1a Mutation

Familial hemiplegic migraine (FHM) and alternating hemiplegia of childhood (AHC) are severe neurological disorders that share clinical features. Therefore, FHM genes are candidates for AHC. We performed mutation analysis in the CACNA1A gene in a monozygotic twin pair with clinical features overlapping with both AHC and FHM and identified a novel de novo CACNA1A mutation. We provide the first evidence that a CACNA1A mutation can cause atypical AHC, indicating an overlap of molecular mechanisms causing AHC and FHM. These results also suggest that CACNA1A mutation scanning is indicated in patients with a severe neurological phenotype that includes paroxysmal (alternating) hemiplegia.

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