Changes In Chromosome Number Research Articles

Evolutionary mechanisms of runaway chromosome number change in Agrodiaetus butterflies

Despite predictions of the classic, hybrid-sterility model of chromosomal speciation, some organisms demonstrate high rate of karyotype evolution. This rate is especially impressive in Agrodiaetus butterflies that rapidly evolved the greatest chromosome number diversity known in animal kingdom within a single subgenus. Here we analyzed karyotype evolution in Agrodiaetus using phylogenetic comparative methods. We found that chromosome numbers possess a strong phylogenetic signal. This disproves the chromosome megaevolution model that proposes multiple chromosome rearrangements to accumulate independently in each of closely related species. We found that Brownian motion gives a more adequate description of observed trait changes than Ornstein-Uhlenbeck model. This indicates that chromosome numbers evolve via random walk along branches of the phylogeny. We discovered a correlation between karyotype changes and phylogeny branch lengths. This gradual pattern is inconsistent with the hybrid-sterility model which, due to association of major chromosome changes with cladogenetic events, predicts a high degree of punctualism in karyotype evolution. Thus, low underdominace of chromosomal rearrangements and/or prevalence of the recombination-suppression model over the hybrid-sterility model of chromosome speciation are the most common engines of the runaway chromosome number change observed.

Evolutionary implications of heterochromatin and rDNA in chromosome number and genome size changes during dysploidy: A case study in Reichardia genus.

In this study we showed that constitutive heterochromatin, GC-rich DNA and rDNA are implicated in chromosomal rearrangements during the basic chromosome number changing (dysploidy) in Reichardia genus. This small Mediterranean genus comprises 8–10 species and presents three basic chromosome numbers (x = 9, 8 and 7). To assess genome evolution and differentiation processes, studies were conducted in a dysploid series of six species: R. dichotoma, R. macrophylla and R. albanica (2n = 18), R. tingitana and R. gaditana (2n = 16), and R. picroides (2n = 14). The molecular phylogeny reconstruction comprised three additional species (R. crystallina and R. ligulata, 2n = 16 and R. intermedia, 2n = 14). Our results indicate that the way of dysploidy is descending. During this process, a positive correlation was observed between chromosome number and genome size, rDNA loci number and pollen size, although only the correlation between chromosome number and genome size is still recovered significant once considering the phylogenetic effect. Fluorescent in situ hybridisation also evidenced changes in number, position and organisation of two rDNA families (35S and 5S), including the reduction of loci number and, consequently, reduction in the number of secondary constrictions and nuclear organising regions from three to one per diploid genome. The potential mechanisms of chromosomal and genome evolution, strongly implicating heterochromatin, are proposed and discussed, with particular consideration for Reichardia genus.

Cladogenetic and Anagenetic Models of Chromosome Number Evolution: A Bayesian Model Averaging Approach.

Chromosome number is a key feature of the higher-order organization of the genome, and changes in chromosome number play a fundamental role in evolution. Dysploid gains and losses in chromosome number, as well as polyploidization events, may drive reproductive isolation and lineage diversification. The recent development of probabilistic models of chromosome number evolution in the groundbreaking work by Mayrose et al. (2010, ChromEvol) have enabled the inference of ancestral chromosome numbers over molecular phylogenies and generated new interest in studying the role of chromosome changes in evolution. However, the ChromEvol approach assumes all changes occur anagenetically (along branches), and does not model events that are specifically cladogenetic. Cladogenetic changes may be expected if chromosome changes result in reproductive isolation. Here we present a new class of models of chromosome number evolution (called ChromoSSE) that incorporate both anagenetic and cladogenetic change. The ChromoSSE models allow us to determine the mode of chromosome number evolution; is chromosome evolution occurring primarily within lineages, primarily at lineage splitting, or in clade-specific combinations of both? Furthermore, we can estimate the location and timing of possible chromosome speciation events over the phylogeny. We implemented ChromoSSE in a Bayesian statistical framework, specifically in the software RevBayes, to accommodate uncertainty in parameter estimates while leveraging the full power of likelihood based methods. We tested ChromoSSE's accuracy with simulations and re-examined chromosomal evolution in Aristolochia, Carex section Spirostachyae, Helianthus, Mimulus sensu lato (s.l.), and Primula section Aleuritia, finding evidence for clade-specific combinations of anagenetic and cladogenetic dysploid and polyploid modes of chromosome evolution. [Anagenetic; Bayes factors; chromosome evolution; chromosome speciation; chromoSSE; cladogenetic; dysploidy; phylogenetic models; polyploidy; reversible-jump Markov chain Monte Carlo; whole genome duplication.].

Genomic markers of ovarian adenocarcinoma and its relevancy to the effectiveness of chemotherapy.

Ovarian cancer is the eighth most common cancer and the seventh highest cause of cancer-associated mortality in women worldwide. It is the second highest cause of mortality among female reproductive malignancies. The current standard first-line treatment for advanced ovarian cancer includes a combination of surgical debulking and standard systemic platinum-based chemotherapy with carboplatin and paclitaxel. Although a deeper understanding of this disease has been attained, relapse occurs in 70% of patients 18 months subsequent to the first-line treatment. Therefore, it is crucial to develop a novel drug that effectively affects ovarian cancer, particularly tumors that are resistant to current chemotherapy. The aim of the present study was to identify genes whose expression may be used to predict survival time or prognosis in ovarian cancer patients treated with chemotherapy. Gene or protein expression is an important issue in chemoresistance and survival prediction in ovarian cancer. In the present study, the research group consisted of patients treated at the Surgical Clinic of the Gynecology and Obstetrics Gynecological Clinical Hospital, Poznan University of Medical Sciences (Poznan, Poland) between May 2006 and November 2014. Additional eligibility criteria were a similar severity (International Federation of Gynecolgy and Obstetrics stage III) at the time of diagnosis, treatment undertaken in accordance with the same schedule, and an extremely good response to treatment or a lack of response to treatment. The performance of the OncoScan® assay was evaluated by running the assay on samples obtained from the four patients and by following the recommended protocol outlined in the OncoScan assay manual. The genomic screening using Affymetrix OncoScan Arrays resulted in the identification of large genomic rearrangements across all cancer tissues. In general, chromosome number changes were detected in all examined tissues. The OncoScan arrays enabled the identification of ~100 common somatic mutations. Chemotherapy response in ovarian cancer is extremely complex and challenging to study. The present study identified specific genetic alterations associated with ovarian cancer, but not with response for treatment.

Variation in genome size in the Valeriana officinalis complex resulting from multiple chromosomal evolutionary processes

Polyploidy, aneuploidy and change in DNA content of monoploid genomes or chromosomes are the principal causes of the variation in genome size. We studied these phenomena in central-European populations of the Valeriana officinalis complex in order to identify mechanisms or forces driving its evolution. The complex comprises di-, tetra- and octoploid morphologically defined so-called taxonomic “types”. Within the study area there are also intermediate “transitional types” the existence of which hampers the application of traditional taxonomic concepts. We thus chose AFLP genotyping and admixture analyses to identify the genetic structuring of the material studied. Di- (2x), tetra- (4x) and octoploidy (8x) were confirmed as major ploidy levels. Major genetic clusters roughly corresponded to these ploidy levels (for K = 2: 2x- and 8x-clusters, for K = 4 with nearly identical probability: 2x-, 4x-, 8x- and unspecific clusters were identified), which further more significantly differed from each other in monoploid absolute genome size (mean 1Cx for 2x = 1.48 pg, 4x 1.29 pg, 8x 1.10 pg). Several individuals of all ploidy levels were admixed, particularly tetraploids. Relative genome size (the sample: standard DAPI fluorescence) was positively correlated with the proportion of the diploid genetic cluster shared by the tetraploids, indicating that hybridization caused the variation in genome size. This result is in accordance with the significant negative correlation of the genome size of tetraploids with their geographic distance to the diploids. However, remarkable intra-ploidy variation in relative genome size was recorded for all ploidy levels (1.14-fold in diploids, 1.28-fold in tetraploids, 1.19-fold in octoploids). We identified aneuploidy as an additional source of variation in genome size in the di- and tetraploids. The contribution of extra chromosomes to absolute genome size exceeded the observed variation within euploids in the diploids, whereas it was included in the regular variability in genome size recorded for the eutetraploids. Variation in monoploid genome size was recorded in polyploids but not in diploids, indicating that polyploids experienced higher dynamics in the evolution of their genomes. Finally, 38.0–63.2% of the total intra-ploidy variation in relative genome size occurred within populations. In conclusion, the Valeriana officinalis complex provides an example of variation in genome size due to four principal evolutionary forces: polyploidization, change in chromosome number and in DNA content of chromosomes and (secondarily) hybridization, but their relative importance differed among ploidy levels. Although the stability in the size of the monoploid genome in species is considered to be the standard case, we found great variability within populations suggesting that genome size is variable even within narrowly defined taxa.

The Cohesin Subunit Rad21 Is a Negative Regulator of Hematopoietic Self-Renewal through Epigenetic Repression of HoxA7 and HoxA9

Abstract Acute myelogenous leukemia (AML) is a high-risk hematopoietic malignancy with a poor prognosis. Developing novel treatments for AML has been difficult due to the heterogeneity of genetic mutations observed across patients. Recent genomic sequencing of AML patients have identified recurrent somatic mutations in cohesin complex genes in a subset of patients (10-20%). The canonical function of the cohesin complex is to maintain sister chromatid cohesion permitting proper segregation of genomic information to each daughter cell in mitosis. Interestingly, somatic cohesin mutations in AML are uniformly heterozygous and not associated with dramatic changes in chromosomal number, implying that cohesin mutations promote AML through a function independent of their role during mitosis. Recent studies have demonstrated that haploinsufficiency of the cohesin complex leads to enhanced self-renewal in Hematopoeitic Stem and Progenitor Cells (HSPCs). We sought to delineate the molecular mechanisms by which cohesin mutations promote enhanced HSPC self-renewal since this represents an early step of oncogenic transformation. In the present study we confirmed previous studies showing that reduced cohesin levels elicit enhanced self-renewal of murine HPSCs in vitro in serial-replating assays. Gene arrays and RT-qPCR identified significant increases in the HSPC self-renewal factors Hoxa7 and Hoxa9. We confirmed the gene array data by RT-PCR and observed that Hoxa9 levels increase within 24 hours following Rad21 depletion. Consistent with these data, multiple approaches demonstrated a high correlation between Rad21 depletion and Hoxa9 target gene expression programs. We next sought to identify the mechanism that leads to this abberant expression of Hoxa9. GSEA identified derepression of Polycomb Repressive Complex 2 (PRC2) target genes in Rad21-depleted HSPCs. Given the well-described silencing of Hox clusters by the PRC2 complex, we examined if Rad21-depletion-induced HoxA9 gene activation could be mediated by epigenetic changes. Rad21 depletion resulted in decreased levels of H3K27me3 at the Hoxa7 and Hoxa9 promoters, indicating that Rad21 plays a role in proper PRC2 mediated silencing of these genes. Using immunoprecipitation experiments we further demonstrate that cohesin and PRC2 interact and are bound in close proximity to Hoxa7 and Hoxa9, arguing that Hoxa7 and Hoxa9 derepression is directly mediated by Rad21-targeting of PRC2. Consistent with this finding we observed reduced global levels of PRC2's repressive histone mark H3K27me3 arguing that PRC2 requires the cohesin complex for proper targeting. Importantly, knockdown of either Hoxa7 or Hoxa9 suppressed self-renewal, implying both are critical downstream effectors of reduced cohesin levels. Interestingly, inhibition of Dot1L function also reduced the enhanced self-renewal capacity elicited by cohesin depletion, consistent with the Hoxa locus being regulated by H3K79 methylation. Our data demonstrate that the cohesin complex regulates PRC2 targeting to silence Hoxa7 and Hoxa9 and negatively regulate self-renewal. Our studies identify a novel epigenetic mechanism underlying leukemogenesis and provide a possible therapeutic treatment for AML patients harboring cohesin mutations. Disclosures No relevant conflicts of interest to declare.

Insights into the phylogeny and evolutionary history of Calyceraceae

AbstractCalyceraceae is a small family with six traditionally recognized genera and 47 species from southern South America. Most species grow along the Andes (of both Argentina and Chile) and in arid regions of the Patagonian steppe. This family belongs to the well‐supported MGCA clade within Asterales, which includes Menyanthaceae+Goodeniaceae+Calyceraceae+ Asteraceae. Calyceraceae is monophyletic and sister to Asteraceae, one of the five largest families of angiosperms. Although Calyceraceae is clearly distinct as a family, its genera are not, and taxonomic revisionary effort has confirmed the lack of sharp boundaries among genera. We performed a phylogenetic analysis of Calyceraceae with a broad taxon sampling (41 of 47 species), and with sequence data from multiple regions from the nuclear (ITS) and plastid genomes (ycg6‐psbM, psbM‐trnD, trnS‐trnG, trnH‐psbA, trnD‐trnT) using maximum parsimony and Bayesian approaches. We aimed at identifying monophylectic groups, their putative morphological synapomorphies and their geographical distribution; we also estimated divergence times and examined chromosomes numbers in an evolutionary context. We obtained well‐resolved and strongly supported phylogenies that show Calyceraceae to be divided into two major clades with geographically structured subclades within each. Our results indicate that an early split within Calyceraceae occurred about 27.4 Ma, probably related to differential changes in chromosome numbers, which allowed the two lineages to evolve in sympatry. We found that major natural subgroups diverged 15–12 Ma, following the Early‐Miocene South Andes construction stage. Finally, the diversification of the extant species is probably associated to Andean orogeny and climate changes in the last 5–4 Myr. We recovered Acicarpha as monophyletic, while the remaining traditionally recognized genera of Calyceraceae are para‐ or polyphyletic. Most species of Moschopis are included in the Glutinose group, but M. monocephala is more closely related to some Calycera species. Calycera is divided into two clades; the Calycera group and the Pilose group. All species of Nastanthus are placed in a well‐supported main group with species of Gamocarpha and Boopis. Gamocarpha could be monophyletic after exclusion of G. dentata and G. angustifolia, but is nested within Nastanthus and Boopis species. Boopis is clearly polyphyletic with its species distributed in all main groups.

The Evolution of Haploid Chromosome Numbers in the Sunflower Family.

Chromosome number changes during the evolution of angiosperms are likely to have played a major role in speciation. Their study is of utmost importance, especially now, as a probabilistic model is available to study chromosome evolution within a phylogenetic framework. In the present study, likelihood models of chromosome number evolution were fitted to the largest family of flowering plants, the Asteraceae. Specifically, a phylogenetic supertree of this family was used to reconstruct the ancestral chromosome number and infer genomic events. Our approach inferred that the ancestral chromosome number of the family is n = 9. Also, according to the model that best explained our data, the evolution of haploid chromosome numbers in Asteraceae was a very dynamic process, with genome duplications and descending dysploidy being the most frequent genomic events in the evolution of this family. This model inferred more than one hundred whole genome duplication events; however, it did not find evidence for a paleopolyploidization at the base of this family, which has previously been hypothesized on the basis of sequence data from a limited number of species. The obtained results and potential causes of these discrepancies are discussed.

The Impact of Reconstruction Methods, Phylogenetic Uncertainty and Branch Lengths on Inference of Chromosome Number Evolution in American Daisies (Melampodium, Asteraceae).

Chromosome number change (polyploidy and dysploidy) plays an important role in plant diversification and speciation. Investigating chromosome number evolution commonly entails ancestral state reconstruction performed within a phylogenetic framework, which is, however, prone to uncertainty, whose effects on evolutionary inferences are insufficiently understood. Using the chromosomally diverse plant genus Melampodium (Asteraceae) as model group, we assess the impact of reconstruction method (maximum parsimony, maximum likelihood, Bayesian methods), branch length model (phylograms versus chronograms) and phylogenetic uncertainty (topological and branch length uncertainty) on the inference of chromosome number evolution. We also address the suitability of the maximum clade credibility (MCC) tree as single representative topology for chromosome number reconstruction. Each of the listed factors causes considerable incongruence among chromosome number reconstructions. Discrepancies between inferences on the MCC tree from those made by integrating over a set of trees are moderate for ancestral chromosome numbers, but severe for the difference of chromosome gains and losses, a measure of the directionality of dysploidy. Therefore, reliance on single trees, such as the MCC tree, is strongly discouraged and model averaging, taking both phylogenetic and model uncertainty into account, is recommended. For studying chromosome number evolution, dedicated models implemented in the program ChromEvol and ordered maximum parsimony may be most appropriate. Chromosome number evolution in Melampodium follows a pattern of bidirectional dysploidy (starting from x = 11 to x = 9 and x = 14, respectively) with no prevailing direction.

Chromosome-wide mechanisms to decouple gene expression from gene dose during sex-chromosome evolution

Changes in chromosome number impair fitness by disrupting the balance of gene expression. Here we analyze mechanisms to compensate for changes in gene dose that accompanied the evolution of sex chromosomes from autosomes. Using single-copy transgenes integrated throughout the Caenorhabditis elegans genome, we show that expression of all X-linked transgenes is balanced between XX hermaphrodites and XO males. However, proximity of a dosage compensation complex (DCC) binding site (rex site) is neither necessary to repress X-linked transgenes nor sufficient to repress transgenes on autosomes. Thus, X is broadly permissive for dosage compensation, and the DCC acts via a chromosome-wide mechanism to balance transcription between sexes. In contrast, no analogous X-chromosome-wide mechanism balances transcription between X and autosomes: expression of compensated hermaphrodite X-linked transgenes is half that of autosomal transgenes. Furthermore, our results argue against an X-chromosome dosage compensation model contingent upon rex-directed positioning of X relative to the nuclear periphery.

Pollinator-Mediated Isolation May Be an Underestimated Factor in Promoting Homoploid Hybrid Speciation

Pollinator-Mediated Isolation May Be an Underestimated Factor in Promoting Homoploid Hybrid Speciation

Induction of genomic instability and activation of autophagy in artificial human aneuploid cells

Chromosome missegregation can lead to a change in chromosome number known as aneuploidy. Although aneuploidy is a known hallmark of cancer cells, the various mechanisms by which altered gene and/or DNA copy number facilitate tumorigenesis remain unclear. To understand the effect of aneuploidy occurring in non-tumorigenic human breast epithelial cells, we generated clones harboring artificial aneuploidy using microcell-mediated chromosome transfer. Our results demonstrate that clones with artificial aneuploidy of chromosome 8 or chromosome 22 both show inhibited proliferation and genomic instability. Also, the increased autophagy was observed in the artificially aneuploidy clones, and inhibition of autophagy resulted in increased genomic instability and DNA damage. In addition, the intracellular levels of reactive oxygen species were up-regulated in the artificially aneuploid clones, and inhibition of autophagy further increased the production of reactive oxygen species. Together, these results suggest that even a single extraneous chromosome can induce genomic instability, and that autophagy triggered by aneuploidy-induced stress is a mechanism to protect cells bearing abnormal chromosome number.

Somaclonal variation in ‘Red Flash’ caladium: morphological, cytological and molecular characterization

Somaclonal variation is a major concern to many applications of plant cell and tissue culture techniques, yet it could be a useful source of variation for plant genetic improvement. High frequencies of somaclonal variants were reported in caladium, but little was known about changes in caladium somaclonal variants at the cellular and molecular levels. Twenty-four somaclonal variants were identified among ‘Red Flash’ caladium plants regenerated from two types of leaf explants and on two media containing different auxins. Results showed that the type of leaf explants and auxin affected the occurrence of somaclonal variants in ‘Red Flash’. The highest percentage of variants (25.0 %) was observed among plants regenerated from mature leaf explants cultured on the media containing 2,4-dichlorophenoxyacetic acid. These somaclonal variants exhibited considerable changes in leaf shape, coloring of the main veins, spots, margins, and leaf size, and could be separated into 10 somaclonal variant groups. Twelve variants contained 1.1–5.4 % less nuclear DNA and appeared to have lost one chromosome. Two variants contained 5.4–9.2 % less nuclear DNA and appeared to have lost two chromosomes. One variant contained 95.0 % more nuclear DNA and 2n = 58 chromosomes. Two SSR markers (CaM1 and CaM103) revealed DNA banding pattern changes in nine variants, including allele loss in eight variants and allele size change in one variant. These results suggested that several cytological and/or molecular causes were involved in the somaclonal variation in ‘Red Flash’ and chromosome number change was a frequent cause leading to a high frequency of aneuploids and marker allele loss. The CaM1-carrying chromosome seemed to be unstable and prone to loss during tissue culture.

Investigating the Mechanism of Wnt‐Induced Chromosomal Instability

Wnt signaling is essential for early embryonic development, the maintenance of stem cell pluripotency, determination of cell polarity, and cellular differentiation. Alterations in Wnt signaling activity have dramatic effects, resulting in developmental defects and contributing to the development of cancer. We recently found that perturbations in Wnt signaling lead to chromosomal instability (CIN), which results in aneuploidy, a hallmark of many cancer cells. However, we currently do not understand the mechanism by which Wnt promotes this CIN. We hypothesize that the protein p53 (gene name = TP53), often described as “the guardian of the genome”, acts downstream of Wnt to influence the fidelity of chromosome segregation. The goals of my research are to further study the effect of Wnt signaling on CIN and to explore the potential involvement of p53 in this process. To this end, I am utilizing DNA fluorescence in situ hybridization (FISH) as a means to detect and quantify the frequency of chromosome mis‐segregation across a population of cells. This method will allow me to detect changes in chromosome numbers in response to Wnt stimulation over time. In addition, I am creating a human embryonic stem cell line (H1/WA01) that will express fusion proteins composed of a fluorescent protein and either a histone (H2B) or tubulin. These transgene expressing H1 cells will be used to visualize mitosis and chromosome mis‐segregation. To address the involvement of p53, I will monitor both changes in gene expression of TP53 and changes in p53 protein abundance and modification, including phosphorylation and acetylation. Any observed changes in TP53 gene expression or p53 protein in response to Wnt signaling may contribute to CIN and hence to the occurrence of aneuploidy. These studies into the mechanism of Wnt‐induced CIN and the role of p53 will provide valuable insights into the development of cancer and may help identify a novel target of cancer therapeutics.Support or Funding InformationThis work is supported by a grant from the CIRM (RB1‐01406, to K.W.) and was made possible in part by the California Institute for Regenerative Medicine (CIRM) Major Facilities Grant (FA1‐00607) to the Sanford Consortium for Regenerative Medicine.

Presumable incipient hybrid speciation of door snails in previously glaciated areas in the Caucasus

Homoploid hybrid speciation, speciation by hybridization without a change in chromosome number, may be the result of an encounter of closely related species in a habitat that is different from that usually occupied by these species. In the northwestern Caucasus the land snail species Micropontica caucasica and M. circassica form two distinct entities with little admixture at low and intermediate altitudes. However, at higher altitudes in the Lagonaki plateau, which were repeatedly glaciated, Micropontica populations with intermediate characters occur. Admixture analyses based on AFLP data demonstrated that the populations from the Lagonaki plateau are homoploid hybrids that now form a cluster separate from the parental species. The Lagonaki populations are characterized by a mtDNA haplotype clade that has been found in the parental species only once. The fixation of this haplotype clade in most hybrid populations suggests that these haplotypes are better adapted to the cooler conditions in high altitude habitats and have replaced the haplotypes of the parental species in a selective sweep. The fixation of a presumably adaptive mitochondrial haplotype clade in the Lagonaki populations is an important step towards speciation under the differential fitness species concept.

Aneuploidy triggers a TFEB-mediated lysosomal stress response

Aneuploidy, defined as an alteration in chromosome number that is not a multiple of the haploid complement, severely affects cellular physiology. Changes in chromosome number lead to imbalances in cellular protein composition, thus disrupting cellular processes and causing proteins to misfold and aggregate. We recently reported that in mammalian cells protein aggregates are readily encapsulated within autophagosomes but are not degraded by lysosomes. This leads to a lysosomal stress response in which the transcription factor TFEB induces expression of factors needed for macroautophagy-mediated protein degradation. Our studies uncover lysosomal degradation defects as a feature of the aneuploid state, and a role for the transcription factor TFEB in the response thereto.

Diploid hybrid origin ofHippophaë gyantsensis(Elaeagnaceae) in the western Qinghai-Tibet Plateau

Homoploid hybrid speciation, the origin of a hybrid species without change in chromosome number, is currently considered to be a rare form of speciation. In the present study, we examined the phylogenetic origin of Hippophaë gyantsensis, a diploid species occurring in the western Qinghai–Tibet Plateau. Some of its morphological and molecular traits suggest a close relationship to H. rhamnoides ssp. yunnanensis while others indicate H. neurocarpa. We conducted phylogenetic analyses of sequence data of two maternally inherited chloroplast (cp) DNA fragments and the bi-parentally inherited nuclear ribosomal internal transcribed spacer (ITS) from 17 populations of H. gyantsensis, 15 populations of H. rhamnoides ssp. yunnanensis and 27 populations of H. neurocarpa across their distributional ranges, and modelled the niche differentiation of the three taxa. Multiple lines of evidence suggested that H. gyantsensis is a morphologically stable, genetically independent and ecologically distinct species. The inconsistent phylogenetic placements of the H. gyantsensis clade that comprised the dominant cpDNA haplotypes and ITS ribotypes suggested a probable diploid hybrid origin from multiple crosses between H. rhamnoides ssp. yunnanensis and H. neurocarpa. This tentative hypothesis is more parsimonious than alternative explanations according to the data available, although more evidence based on further testing is needed.

Is post-polyploidization diploidization the key to the evolutionary success of angiosperms?

Advances in recent years have revolutionized our understanding of both the context and occurrence of polyploidy in plants. Molecular phylogenetics has vastly improved our understanding of plant relationships, enabling us to better understand trait and character evolution, including chromosome number changes. This, in turn, has allowed us to appreciate better the frequent occurrence and extent of polyploidy throughout the history of angiosperms, despite the occurrence of low chromosome numbers in some groups, such as in Arabidopsis (A. thaliana was the first plant genome to be sequenced and assembled). In tandem with an enhanced appreciation of phylogenetic relationships, the accumulation of genomic data has led to the conclusion that all angiosperms are palaeopolyploids, together with better estimates of the frequency and type of polyploidy in different angiosperm lineages. The focus therefore becomes when a lineage last underwent polyploidization, rather than simply whether a plant is ‘diploid’ or ‘polyploid’. This legacy of past polyploidization in plants is masked by large-scale genome reorganization involving repetitive DNA loss, chromosome rearrangements (including fusions and fissions) and complex patterns of gene loss, a set of processes that are collectively termed ‘diploidization’. We argue here that it is the diploidization process that is responsible for the ‘lag phase’ between polyploidization events and lineage diversification. If so, diploidization is important in determining chromosome structure and gene content, and has therefore made a significant contribution to the evolutionary success of flowering plants. © 2015 The Authors. Botanical Journal of the Linnean Society published by John Wiley & Sons Ltd on behalf of The Linnean Society of London, Botanical Journal of the Linnean Society, 2015, ●●, ●●–●●.

Evidence for a conserved karyotype in Swartzia (Fabaceae, Papilionoideae): Implications for the taxonomy and evolutionary diversification of a species-rich neotropical tree genus

To assess the taxonomic utility of cytogenetic variation in the species-rich neotropical papilionoid legume genus Swartzia and to ascertain the importance of cytogenetic evolution in the diversification history of the genus, a variety of cytogenetic data—chromosome number, chromosome lengths, relative chromosome length, total chromatin length (TCL), CMA/DAPI and FISH—were collected for 19 taxa of Swartzia and for a single species of the related genus Ateleia. In the sampled species of Swartzia, chromosome counts yielded a diploid number of 2n=2x=26. However, both diploid and tetraploid (2n=4x=52) counts were obtained for S. leptopetala. The species of Swartzia presented small chromosomes (0.25μm to 1.41μm), with gradual length variation, furthermore, each of them had two sites of CMA+/DAPI- and two sites of 45S and 5S rDNA. Cytogenetic data for the morphologically anomalous species S. euxylophora convey its close relationship to other species of Swartzia. Ateleia ovata was found to differ from all of the sampled taxa of Swartzia in diploid chromosome number (2n =28). Taken together, these results constitute preliminary evidence for a strongly conserved karyotype pattern in Swartzia and in combination with previously published data suggest that karyological characters, while useful for characterizing the genus, are of limited taxonomic utility within Swartzia. We conclude that cytogenetic evolution involving changes in chromosome number has not figured prominently in the explosive diversification history of Swartzia.

Evolutionary analysis identifies multiple genome expansions and contractions in Sepsidae (Diptera) and suggests targets for future genomic research.

We here argue that data from comparative studies of genome size and karyotypes provide important information for planning comparative research on genome evolution. We document for 39 species of sepsids that there is a four-fold difference in genome size (151-618 Mbp). Mapping genome sizes onto a phylogenetic hypothesis identifies that this range is the result of five genome expansions and four genome contractions that we here define as changes in genome size of more than 50 Mbp. We then generate karyotype data for 10 species and find no changes in chromosome number. The study reveals that the "Oriental" clade of sepsids is a promising system for studying genome evolution because it has experienced three genome expansion events. These events can be compared with an expansion in the "Neotropical" clade in order to reveal the mechanisms that underlie genome expansion in Sepsidae. A review of the literature on genome sizes and karyotypes reveals that they have been poorly documented in Metazoa. This means that researchers interested in the evolution of genome expansions and contractions are currently not being able to identify appropriate target taxa for genome sequencing. We thus argue for more comparative research on genome sizes and karyotypes and point out that historically species were chosen for genome sequencing for reasons not related to genome evolution (e.g. small genome size, model species status, phylogenetic position, interesting phenotypes). We believe that it is now time to use a more genome-centric selection criterion, where species for whole genome sequencing are selected based on their importance for understanding genome evolution.