Changes In Chromosome Number Research Articles

Chromosome aberrations induced by the non-mutagenic carcinogen acetamide involve in rat hepatocarcinogenesis through micronucleus formation in hepatocytes.

Chromosome aberrations (CAs), i.e. changes in chromosome number or structure, are known to cause chromosome rearrangements and subsequently tumorigenesis. However, the involvement of CAs in chemical-induced carcinogenesis is unclear. In the current study, we aimed to clarify the possible involvement of CAs in chemical carcinogenesis using a rat model with the non-mutagenic hepatocarcinogen acetamide. In an in vivo micronucleus (MN) test, acetamide was revealed to induce CAs specifically in rat liver at carcinogenic doses. Acetamide also induced centromere-positive large MN (LMN) in hepatocytes. Immunohistochemical and electron microscopic analyses of the LMN, which can be histopathologically detected as basophilic cytoplasmic inclusion, revealed abnormal expression of nuclear envelope proteins, increased heterochromatinization, and massive DNA damage. These molecular pathological features in LMN progressed with acetamide exposure in a time-dependent manner, implying that LMN formation can lead to chromosome rearrangements. Overall, these data suggested that CAs induced by acetamide play a pivotal role in acetamide-induced hepatocarcinogenesis in rats and that CAs can cause chemical carcinogenesis in animals via MN formation.

Chromosome Fusion Affects Genetic Diversity and Evolutionary Turnover of Functional Loci but Consistently Depends on Chromosome Size.

Major changes in chromosome number and structure are linked to a series of evolutionary phenomena, including intrinsic barriers to gene flow or suppression of recombination due to chromosomal rearrangements. However, chromosome rearrangements can also affect the fundamental dynamics of molecular evolution within populations by changing relationships between linked loci and altering rates of recombination. Here, we build chromosome-level assembly Eueides isabella and, together with a recent chromosome-level assembly of Dryas iulia, examine the evolutionary consequences of multiple chromosome fusions in Heliconius butterflies. These assemblies pinpoint fusion points on 10 of the 20 autosomal chromosomes and reveal striking differences in the characteristics of fused and unfused chromosomes. The ten smallest autosomes in D. iulia and E. isabella, which have each fused to a longer chromosome in Heliconius, have higher repeat and GC content, and longer introns than predicted by their chromosome length. When fused, these characteristics change to become more in line with chromosome length. The fusions also led to reduced diversity, which likely reflects increased background selection and selection against introgression between diverging populations, following a reduction in per-base recombination rate. We further show that chromosome size and fusion impact turnover rates of functional loci at a macroevolutionary scale. Together these results provide further evidence that chromosome fusion in Heliconius likely had dramatic effects on population level processes shaping rates of neutral and adaptive divergence. These effects may have impacted patterns of diversification in Heliconius, a classic example of an adaptive radiation.

SOG1 transcription factor promotes the onset of endoreduplication under salinity stress in Arabidopsis

As like in mammalian system, the DNA damage responsive cell cycle checkpoint functions play crucial role for maintenance of genome stability in plants through repairing of damages in DNA and induction of programmed cell death or endoreduplication by extensive regulation of progression of cell cycle. ATM and ATR (ATAXIA-TELANGIECTASIA-MUTATED and -RAD3-RELATED) function as sensor kinases and play key role in the transmission of DNA damage signals to the downstream components of cell cycle regulatory network. The plant-specific NAC domain family transcription factor SOG1 (SUPPRESSOR OF GAMMA RESPONSE 1) plays crucial role in transducing signals from both ATM and ATR in presence of double strand breaks (DSBs) in the genome and found to play crucial role in the regulation of key genes involved in cell cycle progression, DNA damage repair, endoreduplication and programmed cell death. Here we report that Arabidopsis exposed to high salinity shows generation of oxidative stress induced DSBs along with the concomitant induction of endoreduplication, displaying increased cell size and DNA ploidy level without any change in chromosome number. These responses were significantly prominent in SOG1 overexpression line than wild-type Arabidopsis, while sog1 mutant lines showed much compromised induction of endoreduplication under salinity stress. We have found that both ATM-SOG1 and ATR-SOG1 pathways are involved in the salinity mediated induction of endoreduplication. SOG1was found to promote G2-M phase arrest in Arabidopsis under salinity stress by downregulating the expression of the key cell cycle regulators, including CDKB1;1, CDKB2;1, and CYCB1;1, while upregulating the expression of WEE1 kinase, CCS52A and E2Fa, which act as important regulators for induction of endoreduplication. Our results suggest that Arabidopsis undergoes endoreduplicative cycle in response to salinity induced DSBs, showcasing an adaptive response in plants under salinity stress.

The fitness costs and benefits of trisomy of each Candida albicans chromosome.

Candida albicans is a prevalent human fungal pathogen. Rapid genomic change, due to aneuploidy, is a common mechanism that facilitates survival from multiple types of stresses including the few classes of available antifungal drugs. The stress survival of aneuploids occurs despite the fitness costs attributed to most aneuploids growing under idealized lab conditions. Systematic study of the aneuploid state in C. albicans has been hindered by the lack of a comprehensive collection of aneuploid strains. Here, we describe a collection of diploid C. albicans aneuploid strains, each carrying one extra copy of each chromosome, all from the same genetic background. We tested the fitness of this collection under several physiological conditions including shifts in pH, low glucose, oxidative stress, temperature, high osmolarity, membrane stress, and cell wall stress. We found that most aneuploids, under most conditions, were less fit than their euploid parent, yet there were specific conditions under which specific aneuploid isolates provided a fitness benefit relative to the euploid parent strain. Importantly, this fitness benefit was attributable to the change in the copy number of specific chromosomes. Thus, C. albicans can tolerate aneuploidy of each chromosome and some aneuploids confer improved growth under conditions that the yeast encounters in its host niches.

Reduced SKP1 and CUL1 expression underlies increases in Cyclin E1 and chromosome instability in cellular precursors of high-grade serous ovarian cancer

BackgroundHigh-grade serous ovarian cancer (HGSOC) is the most common and lethal ovarian cancer histotype. Chromosome instability (CIN, an increased rate of chromosome gains and losses) is believed to play a fundamental role in the development and evolution of HGSOC. Importantly, overexpression of Cyclin E1 protein induces CIN, and genomic amplification of CCNE1 contributes to HGSOC pathogenesis in ~20% of patients. Cyclin E1 levels are normally regulated in a cell cycle-dependent manner by the SCF (SKP1–CUL1–FBOX) complex, an E3 ubiquitin ligase that includes the proteins SKP1 and CUL1. Conceptually, diminished SKP1 or CUL1 expression is predicted to underlie increases in Cyclin E1 levels and induce CIN.MethodsThis study employs fallopian tube secretory epithelial cell models to evaluate the impact diminished SKP1 or CUL1 expression has on Cyclin E1 and CIN in both short-term (siRNA) and long-term (CRISPR/Cas9) studies.ResultsSingle-cell quantitative imaging microscopy approaches revealed changes in CIN-associated phenotypes and chromosome numbers and increased Cyclin E1 in response to diminished SKP1 or CUL1 expression.ConclusionsThese data identify SKP1 and CUL1 as novel CIN genes in HGSOC precursor cells that may drive early aetiological events contributing to HGSOC development.

Rapid radiation of angraecoids (Orchidaceae, Angraecinae) in tropical Africa characterised by multiple karyotypic shifts under major environmental instability

Angraecoid orchids present a remarkable diversity of chromosome numbers, which makes them a highly suitable system for exploring the impact of karyotypic changes on cladogenesis, diversification and morphological differentiation. We compiled an annotated cytotaxonomic checklist for 126 species of Angraecinae, which was utilised to reconstruct chromosomal evolution using a newly-produced, near-comprehensive phylogenetic tree that includes 245 angraecoid taxa. In tandem with this improved phylogenetic framework, using combined Bayesian, maximum likelihood and parsimony approaches on ITS-1 and five plastid markers, we propose a new cladistic nomenclature for the angraecoids, and we estimate a new timeframe for angraecoid radiation based on a secondary calibration, and calculate diversification rates using a Bayesian approach. Coincident divergence dates between clades with identical geographical distributions in the angraecoids and the pantropical orchid genus Bulbophyllum suggest that the same events may have intervened in the dispersal of these two epiphytic groups between Asia, continental Africa, Madagascar and the Neotropics. The major angraecoid lineages probably began to differentiate in the Middle Miocene, and most genera and species emerged respectively around the Late Miocene-Pliocene boundary and the Pleistocene. Ancestral state reconstruction using maximum likelihood estimation revealed an eventful karyotypic history dominated by descending dysploidy. Karyotypic shifts seem to have paralleled cladogenesis in continental tropical Africa, where approximately 90% of the species have descended from at least one inferred transition from n = 17–18 to n = 25 during the Middle Miocene Climatic Transition, followed by some clade-specific descending and ascending dysploidy from the Late Miocene to the Pleistocene. Conversely, detected polyploidy is restricted to a few species lineages mostly originating during the Pleistocene. No increases in net diversification could be related to chromosome number changes, and the apparent net diversification was found to be highest in Madagascar, where karyotypic stasis predominates. Finally, shifts in chromosome number appear to have paralleled the evolution of rostellum structure, leaflessness, and conspicuous changes in floral colour.

A mixed ploidy natural population of Amorphophallus muelleri provides an opportunity to trace the evolution of Amorphophallus karyotype

Amorphophallus, a perennial herb belongs to the family Araceae, and is widely distributed in Asia and Africa. As an agricultural crop, it has been cultivated and consumed for ~2000 years in China. Previous studies have found that there are chromosome number and ploidy changes in this genus, but there are a few reports on the evolution of different karyotypes. For this study, we collected 37 samples of a wild population of Amorphophallus muelleri from Myanmar and analysed their karyotypes. The karyotype analysis showed that it is a population with mixed chromosome numbers and ploidy, with four karyotypes of 2n = 24, 26, 28 and 39. Combining the results of this study with previous literature, we speculate that karyotypes with 2n = 26 may be the common ancestor, and further the other three karyotypes were evolved from this by various ways. As far as we know, this is the first attempt to put forward the hypothesis of the evolution of those four karyotypes together. On the other hand, by using inter-simple sequence repeat marker-based unweighted pair group method with arithmetic mean cluster analysis, we found that these individuals of four karyotypes can be divided into four corresponding categories, indicating that they have been differentiated at the genome, providing a theoretical basis for future use of these wild germplasm resources.

DNA Damage Response in Multiple Myeloma: The Role of the Tumor Microenvironment.

Simple SummaryMultiple myeloma (MM) is a plasma cell malignancy. Novel therapies have improved outcomes in MM patients; however, MM still remains incurable. MM cells present genomic instability, whose molecular basis is not fully understood. Recently, it has been reported that the DNA damage response (DDR) may influence genomic changes and drug resistance in MM. An abnormal DNA repair function may provide an alternative explanation for genomic instability. In this review, we show an overview of the DNA repair pathways and discuss the role of the tumor microenvironment in governing the DNA repair mechanisms. The tumor microenvironment factors, such as hypoxia and inflammation, and chemotherapeutic agents profoundly influence the DNA repair pathways in MM.Multiple myeloma (MM) is an incurable plasma cell malignancy characterized by genomic instability. MM cells present various forms of genetic instability, including chromosomal instability, microsatellite instability, and base-pair alterations, as well as changes in chromosome number. The tumor microenvironment and an abnormal DNA repair function affect genetic instability in this disease. In addition, states of the tumor microenvironment itself, such as inflammation and hypoxia, influence the DNA damage response, which includes DNA repair mechanisms, cell cycle checkpoints, and apoptotic pathways. Unrepaired DNA damage in tumor cells has been shown to exacerbate genomic instability and aberrant features that enable MM progression and drug resistance. This review provides an overview of the DNA repair pathways, with a special focus on their function in MM, and discusses the role of the tumor microenvironment in governing DNA repair mechanisms.

The karyotype of Adenia and the origin of the base number x = 12 in Passifloroideae (Passifloraceae).

Adenia is an Old World genus of Passifloroideae closely related to Passiflora. The two genera comprise the large majority of Passifloroideae species, although most studies are concentrated on Passiflora. Cytological analyses reveal that changes in chromosome numbers played an important role in the evolution of Passiflora, whereas in the remaining genera little is known, hindering the identification of the base number of the family. Here we analyzed the chromosome number and the 35S rDNA sites of three species of Adenia and reevaluated the base number (x) of the subfamily Passifloroideae and the family Passifloraceae, including chromosome data for Turneroideae and Malesherbioideae. The chromosome number of Adenia species seemed to be stable with 2n = 24 or 48 and one or two pairs of rDNA sites, very similar to Passiflora subgenus Astrophea, suggesting a common ancestral karyotype with x = 12. Differently, Turneroideae and Malesherbioideae present x = 7. A whole genomic duplication detected after the separation of Passifloroideae and Malesherbioideae suggests that the base number of Passifloraceae most probably was x = 7, which by dysploidy and polyploidy generated x = 12 for the subfamily Passifloroideae.

Chromogenic In Situ Hybridization (CISH) as a Method for Detection of C-Myc Amplification in Formalin-Fixed Paraffin-Embedded Tumor Tissue: An Update.

In situ hybridization (ISH) allows evaluation of genetic abnormalities, such as changes in chromosome number, chromosome translocations, or gene amplifications, by hybridization of tagged DNA (or RNA) probes with complementary DNA (or RNA) sequences in interphase nuclei of target tissue. However, chromogenic in situ hybridization (CISH) is also applicable to formalin-fixed, paraffin-embedded (FFPE ) tissues, besides metaphase chromosome spreads. CISH is similar to fluorescent in situ hybridization (FISH) regarding pretreatments and hybridization protocols but differs in the way of visualization. Indeed, CISH signal detection is similar to that used in immunohistochemistry, making use of a peroxidase-based chromogenic reaction instead of fluorescent dyes. In particular, tagged DNA probes are indirectly detected using an enzyme-conjugated antibody targeting the tags. The enzymatic reaction of the chromogenic substrate leads to the formation of strong permanent brown signals that can be visualized by bright-field microscopy at 40× magnification. The advantage of CISH is that it allows the simultaneous observation of gene amplification and tissue morphology, and the slides can be stored for a long time.

Reduced RBX1 expression induces chromosome instability and promotes cellular transformation in high-grade serous ovarian cancer precursor cells.

Despite high-grade serous ovarian cancer (HGSOC) being the most common and lethal gynecological cancer in women, the early etiological events driving disease development remain largely unknown. Emerging evidence now suggests that chromosome instability (CIN; ongoing changes in chromosome numbers) may play a central role in the development and progression of HGSOC. Importantly, genomic amplification of the Cyclin E1 gene (CCNE1) contributes to HGSOC pathogenesis in ~20% of patients, while Cyclin E1 overexpression induces CIN in model systems. Cyclin E1 levels are normally regulated by the SCF (SKP1-CUL1-FBOX) complex, an E3 ubiquitin ligase that includes RBX1 as a core component. Interestingly, RBX1 is heterozygously lost in ~80% of HGSOC cases and reduced expression corresponds with worse outcomes, suggesting it may be a pathogenic event. Using both short (siRNA) and long (CRISPR/Cas9) term approaches, we show that reduced RBX1 expression corresponds with significant increases in CIN phenotypes in fallopian tube secretory epithelial cells, a cellular precursor of HGSOC. Moreover, reduced RBX1 expression corresponds with increased Cyclin E1 levels and anchorage-independent growth. Collectively, these data identify RBX1 as a novel CIN gene with pathogenic implications for HGSOC.

The chromosome-level genome sequence and karyotypic evolution of Megadenia pygmaea (Brassicaceae).

Karyotypic changes in chromosome number and structure are drivers in the divergent evolution of diverse plant species and lineages. This study aimed to reveal the origins of the unique karyotype (2n=12) and phylogenetic relationships of the genus Megadenia (Brassicaceae). A high-quality chromosome-scale genome was assembled for Megadenia pygmaea using Nanopore long reads and high-throughput chromosome conformation capture (Hi-C). The assembled genome is 215.2Mb and is anchored on six pseudochromosomes. We annotated a total of 25,607 high-confidence protein-coding genes and corroborated the phylogenetic affinity of Megadenia with the Brassicaceae expanded lineage II, containing numerous agricultural crops. We dated the divergence of Megadenia from its closest relatives to 27.04 (19.11-36.60) million years ago. A reconstruction of the chromosomal composition of the species was performed based on the de novo assembled genome and comparative chromosome painting analysis. The karyotype structure of M. pygmaea is very similar to the previously inferred proto-Calepineae karyotype (PCK; n=7) of the lineage II. However, an end-to-end translocation between two ancestral chromosomes reduced the chromosome number from n=7 to n=6 in Megadenia. Our reference genome provides fundamental information for karyotypic evolution and evolutionary study of this genus.

Hybrid speciation via inheritance of alternate alleles of parental isolating genes

It is increasingly realized that homoploid hybrid speciation (HHS), which involves no change in chromosome number, is an important mechanism of speciation. HHS will likely increase in frequency as ecological and geographical barriers between species are continuing to be disrupted by human activities. HHS requires the establishment of reproductive isolation between a hybrid and its parents, but the underlying genes and genetic mechanisms remain largely unknown. In this study, we reveal by integrated approaches that reproductive isolation originates in one homoploid hybrid plant species through the inheritance of alternate alleles at genes that determine parental premating isolation. The parent species of this hybrid species are reproductively isolated by differences in flowering time and survivorship on soils containing high concentrations of iron. We found that the hybrid species inherits alleles of parental isolating major genes related to flowering time from one parent and alleles of major genes related to iron tolerance from the other parent. In this way, it became reproductively isolated from one parent by the difference in flowering time and from the other by habitat adaptation (iron tolerance). These findings and further modeling results suggest that HHS may occur relatively easily via the inheritance of alternate parental premating isolating genes and barriers.

Abstract PO-069: Characterizing cell-to-cell heterogeneity and chromosome instability induced by USP22 deficiency in colorectal cancer

Abstract Chromosome instability (CIN) is an aberrant phenotype characterized by an increased rate of gains and losses of chromosomes. CIN is observed in most cancer types, including 85% of colorectal cancer (CRC) cases. Although CIN is a driver of tumor heterogeneity and associated with drug resistance and poor patient prognosis, the genetic defects underlying CIN remain poorly understood. Ubiquitin Specific Peptidase 22 (USP22) is a deubiquitinating enzyme that targets mono-ubiquitin on lysine 120 of histone H2B (H2Bub1). H2Bub1 is a dynamic post-translational modification that modulates chromatin compaction. Importantly, homozygous or heterozygous USP22 deletion is observed in 45% of CRC cases, suggesting this may be a pathogenic event promoting CRC progression. Accordingly, we sought to characterize the impact reduced USP22 expression has on CIN. To reduce USP22 expression in karyotypically stable CRC (HCT116) and immortalized fibroblast (hTERT) cell lines, we employed transient siRNA silencing and stable CRISPR-Cas9 knockout (KO) models. Single-cell quantitative image-based analyses were utilized to monitor CIN-associated phenotypes, including changes in nuclear areas, micronucleus formation and chromosome numbers. In HCT116, USP22 silencing induced CIN phenotypes and an increase in H2Bub1 abundance in mitotic chromosomes. Subsequent mechanistic studies determined that this is accompanied by an increase in the recruitment of the spindle assembly checkpoint kinase BUB1 at metaphase centromeres and an increased frequency of lagging chromosomes in anaphase. Collectively, these data suggest that reduced USP22 expression alters H2Bub1 regulation in mitosis, which impairs mitotic fidelity, thereby inducing CIN. In addition, to assess the relevance of reduced USP22 expression in a distinct cellular context, the impact of USP22 silencing was assessed in hTERT, revealing similar CIN phenotypes, including changes in nuclear area and chromosome numbers. To assess the long-term impact USP22 deletions have on CIN, novel homozygous and heterozygous USP22-KO HCT116 clones were generated and monitored for three months, which revealed dynamic CIN phenotypes and ongoing changes in chromosome complements relative to controls. Collectively, these data identify USP22 as a novel CIN gene and indicate that USP22 deletions in cancer may drive intra-tumor genetic heterogeneity and thereby promote oncogenesis. Citation Format: Lucile M. Jeusset, Zelda D. Lichtensztejn, Kirk J. McManus. Characterizing cell-to-cell heterogeneity and chromosome instability induced by USP22 deficiency in colorectal cancer [abstract]. In: Proceedings of the AACR Virtual Special Conference on Tumor Heterogeneity: From Single Cells to Clinical Impact; 2020 Sep 17-18. Philadelphia (PA): AACR; Cancer Res 2020;80(21 Suppl):Abstract nr PO-069.

The Evolution of Chromosome Numbers: Mechanistic Models and Experimental Approaches.

Chromosome numbers have been widely used to describe the most fundamental genomic attribute of an organism or a lineage. Although providing strong phylogenetic signal, chromosome numbers vary remarkably among eukaryotes at all levels of taxonomic resolution. Changes in chromosome numbers regularly serve as indication of major genomic events, most notably polyploidy and dysploidy. Here, we review recent advancements in our ability to make inferences regarding historical events that led to alterations in the number of chromosomes of a lineage. We first describe the mechanistic processes underlying changes in chromosome numbers, focusing on structural chromosomal rearrangements. Then, we focus on experimental procedures, encompassing comparative cytogenomics and genomics approaches, and on computational methodologies that are based on explicit models of chromosome-number evolution. Together, these tools offer valuable predictions regarding historical events that have changed chromosome numbers and genome structures, as well as their phylogenetic and temporal placements.

Chromosome number evolves at equal rates in holocentric and monocentric clades.

Despite the fundamental role of centromeres two different types are observed across plants and animals. Monocentric chromosomes possess a single region that function as the centromere while in holocentric chromosomes centromere activity is spread across the entire chromosome. Proper segregation may fail in species with monocentric chromosomes after a fusion or fission, which may lead to chromosomes with no centromere or multiple centromeres. In contrast, species with holocentric chromosomes should still be able to safely segregate chromosomes after fusion or fission. This along with the observation of high chromosome number in some holocentric clades has led to the hypothesis that holocentricity leads to higher rates of chromosome number evolution. To test for differences in rates of chromosome number evolution between these systems, we analyzed data from 4,393 species of insects in a phylogenetic framework. We found that insect orders exhibit striking differences in rates of fissions, fusions, and polyploidy. However, across all insects we found no evidence that holocentric clades have higher rates of fissions, fusions, or polyploidy than monocentric clades. Our results suggest that holocentricity alone does not lead to higher rates of chromosome number changes. Instead, we suggest that other co-evolving traits must explain striking differences between clades.

Antagonistic effects of whole-genome duplications and dysploidy on genome sizes in the pantropical monocot family Marantaceae: Consequences in the light of a new molecular phylogeny

Changes in chromosome number and structure, as well as alterations in genome size, are important cytological characters that often reflect speciation events. Due to a wide variety of previously reported chromosome numbers the species-rich arrowroot family (Marantaceae) is an ideal system to investigate the role of chromosomal changes in species diversification, especially of dysploidy and polyploidy. The mechanisms and direction of changes during evolution as well as ancestral states of chromosomal characters are largely unknown. This study provides a detailed survey of chromosomal and genome size variation in 43 Marantaceae accessions (37 species, 16 genera) from the whole distribution range. Phylogenetic tree mapping suggests that x = 13 is the ancestral basic chromosome number. Descending dysploidy to x = 9, 10, 11, and 12 occurred ten times in parallel within each of the five main clades. In contrast, ascending dysploidy to x = 14, occurred only once. Ploidy level variation was confined to basic numbers x = 9, 11, and 13 and was observed in four out of the five clades. The occurrence of triploids and pentaploids points towards heteroploid diploid-tetraploid and tetraploid-hexaploid hybridizations. Trends in genome evolution as exposed by regression analyses revealed a massive genome size increase after dysploidy - and a genome size decrease after polyploidy. A schematic illustration of possible origins and the modes of chromosomal changes in a biogeographical context is presented. Exemplified by the family Marantaceae, it is shown how variable chromosomal evolution can be and how it contributes to species richness and speciation in the plant kingdom.

Genome Size and Chromosome Number Evolution in Korean Iris L. Species (Iridaceae Juss.)

Chromosome numbers, karyotypes, and genome sizes of 14 Iris L. (Iridaceae Juss.) species in Korea and their closely related taxon, Sisyrinchium rosulatum, are presented and analyzed in a phylogenetic framework. To date, understanding the chromosomal evolution of Korean irises has been hampered by their high chromosome numbers. Here, we report analyses of chromosome numbers and karyotypes obtained via classic Feulgen staining and genome sizes measured using flow cytometry in Korean irises. More than a two-fold variation in chromosome numbers (2n = 22 to 2n = 50) and over a three-fold genome size variation (2.39 pg to 7.86 pg/1 C) suggest the putative polyploid and/or dysploid origin of some taxa. Our study demonstrates that the patterns of genome size variation and chromosome number changes in Korean irises do not correlate with the phylogenetic relationships and could have been affected by different evolutionary processes involving polyploidy or dysploidy. This study presents the first comprehensive chromosomal and genome size data for Korean Iris species. Further studies involving molecular cytogenetic and phylogenomic analyses are needed to interpret the mechanisms involved in the origin of chromosomal variation in the Iris.

Rapid homoploid hybrid speciation in British gardens: The origin of Oxford ragwort (Senecio squalidus).

Hybridisation can lead to homoploid hybrid speciation, i.e., the origin of new species without change in chromosome number between parents and offspring. Central to homoploid hybrid speciation is the role of hybridisation in the establishment of reproductive isolation between the hybrid and the parental species in the early stages of speciation, when typically all species occur at least partly in sympatry. In this work we analyse genome-wide polymorphism data obtained by transcriptome sequencing of the British hybrid species Oxford ragwort (Senecio squalidus, Asteraceae), its two Italian parental species (S. aethnensis and S. chrysanthemifolius) and their naturally occurring hybrids on Mt Etna (Italy). We show that Oxford ragwort most likely originated from de novo hybridisation between its two Italian parental species whilst they were in cultivation in British gardens at the turn of the 18th century. Reproductive isolation between the new hybrid species and its parental species probably resulted from inheritance of genetic incompatibilities between the two parental species and subsequent ecological segregation - both of which have been shown in previous studies. Our results imply that S. squalidus meets the most stringent criteria set forth to identify homoploid hybrid speciation, and call attention to the creative role of hybridisation in responding to novel environmental conditions.

Evolutionary impact of whole genome duplication in Poaceae family

Whole genome duplication (WGD) is a common phenomenon in plants, inducing species diversity, promoting speciation, and playing an important role in providing new genetic material in plant evolution. So far, numerous new gene functions such as pseudogenization, neofunctionalization, and subfunctionalization have evolved through WGD. WGD has occurred several times during the evolution of angiosperms over the past 200 million years. Poaceae, one of the largest plant families in the angiosperms, is considered one of the most economically important and ecologically successful plants, with approximately 600 genera and 10,000 species. Many genetic studies have been conducted on these plants. However, study of the most active phylogeny in the Poaceae family study has not yet been completed. Through comparative studies of major Poaceae groups, this review focuses on the effects of genome duplication in the Poaceae family on its evolutionary history and the changes in chromosome numbers.