Loss Of Centromere Research Articles

Comparative genomics of the closely related fungal genera Cryptococcus and Kwoniella reveals karyotype dynamics and suggests evolutionary mechanisms of pathogenesis.

In exploring the evolutionary trajectories of both pathogenesis and karyotype dynamics in fungi, we conducted a large-scale comparative genomic analysis spanning the Cryptococcus genus, encompassing both global human fungal pathogens and nonpathogenic species, and related species from the sister genus Kwoniella. Chromosome-level genome assemblies were generated for multiple species, covering virtually all known diversity within these genera. Although Cryptococcus and Kwoniella have comparable genome sizes (about 19.2 and 22.9 Mb) and similar gene content, hinting at preadaptive pathogenic potential, our analysis found evidence of gene gain (via horizontal gene transfer) and gene loss in pathogenic Cryptococcus species, which might represent evolutionary signatures of pathogenic development. Genome analysis also revealed a significant variation in chromosome number and structure between the 2 genera. By combining synteny analysis and experimental centromere validation, we found that most Cryptococcus species have 14 chromosomes, whereas most Kwoniella species have fewer (11, 8, 5, or even as few as 3). Reduced chromosome number in Kwoniella is associated with formation of giant chromosomes (up to 18 Mb) through repeated chromosome fusion events, each marked by a pericentric inversion and centromere loss. While similar chromosome inversion-fusion patterns were observed in all Kwoniella species with fewer than 14 chromosomes, no such pattern was detected in Cryptococcus. Instead, Cryptococcus species with less than 14 chromosomes showed reductions primarily through rearrangements associated with the loss of repeat-rich centromeres. Additionally, Cryptococcus genomes exhibited frequent interchromosomal translocations, including intercentromeric recombination facilitated by transposons shared between centromeres. Overall, our findings advance our understanding of genetic changes possibly associated with pathogenicity in Cryptococcus and provide a foundation to elucidate mechanisms of centromere loss and chromosome fusion driving distinct karyotypes in closely related fungal species, including prominent global human pathogens.

Syndromic MEN1 parathyroid adenomas consist of both subclonal nodules and clonally independent tumors

Primary hyperparathyroidism with parathyroid tumors is a typical manifestation of Multiple Endocrine Neoplasia Type 1 (MEN1) and is historically termed “primary hyperplasia”. Whether these tumors represent a multi-glandular clonal disease or hyperplasia has not been robustly proven so far. Loss of Menin protein expression is associated with inactivation of both alleles and a good surrogate for a MEN1 gene mutation. The cyclin-dependent kinase inhibitor 1B (CDKN1B) gene is mutated in MEN4 and encodes for protein p27 whose expression is poorly studied in the syndromic MEN1 setting.Here, we analyzed histomorphology and protein expression of Menin and p27 in parathyroid adenomas of 25 patients of two independent, well-characterized MEN1 cohorts. The pattern of loss of heterozygosity (LOH) was assessed by fluorescence in situ hybridization (FISH) in one MEN1-associated parathyroid adenoma. Further, next-generation sequencing (NGS) was performed on eleven nodules of four MEN1 patients.Morphologically, the majority of MEN1 adenomas consisted of multiple distinct nodules, in which Menin expression was mostly lost and p27 protein expression reduced. FISH analysis revealed that most nodules exhibited MEN1 loss, with or without the loss of centromere 11. NGS demonstrated both subclonal evolution and the existence of clonally unrelated tumors.Syndromic MEN1 parathyroid adenomas therefore consist of multiple clones with subclones, which supports the current concept of the novel WHO classification of parathyroid tumors (2022). p27 expression was lost in a large fraction of MEN1 parathyroids and must therefore be used with caution in suggesting MEN4.

Dynamic Regulation of Histone Acetylation By Nuclear Proteolysis Controls Cell Cycle Gene Expression and Chromosome Integrity in Multiple Myeloma

Transcription factors are generally short-lived proteins that undergo active turnover. The dynamic interaction of transcription factors and co-regulators with promoters and enhancers allows cells to continuously adjust gene expression. Whereas the composition and binding of transcription factors at genomic sites is the focus of a widespread research effort, relatively little is known about how these complexes are being removed by the ubiquitin-proteasome system (UPS).Multiple myeloma (MM), the second most common hematopoietic malignancy, has become a model disease for drugs that interfere with the UPS through either blocking or facilitating protein elimination. The proteasome inhibitor Bortezomib, for instance, is used as first-line treatment in myeloma; yet, the process by which myeloma cells are killed by this drug is ill-defined. Since transcription factors are prime targets of proteasomal degradation, our research is focused on defining how proteolysis regulates transcriptional dynamics in this disease and determining the therapeutic relevance for treatment with proteasome inhibitors.Following proteasome inhibition in multiple myeloma cell lines, we performed chromatin-immunoprecipitation for histone H3 acetylation (K27) and multiple histone deacetylases and used next generation sequencing (ChIP-seq) to identify unique gene clusters that are actively regulated by the proteasome and quantify epigenetic changes in dependence of protein turnover. Our findings reveal that cell cycle genes, particularly subsets of genes involved in centromere formation and sister chromatid segregation during mitosis, are associated with nuclear protein turnover and are transcriptionally repressed by proteasome inhibition. Notably, proteasome inhibition increased the recruitment of specific histone deacetylases (HDACs) to the promoters of genes involved in centromere formation. We are investigating the mechanisms for UPS regulation of HDAC abundance at specific genomic locations. Moreover, data analysis of a panel of multiple myeloma patients shows that the expression levels of HDACs correlate with patient survival, specifically when treated with proteasome inhibitors. We are currently exploring how histone modifications and proteasome activity crosstalk in a therapeutically relevant manner in multiple myeloma.Finally, to determine whether epigenetic regulation of centromere stability might play a role in sensitivity or the development of resistance to proteasome inhibitors, we established and optimized long-term treatment of multiple myeloma cell lines with low doses of proteasome inhibitors. Remarkably, we observed reduced immunofluorescence staining for centromeric protein A (CENP-A) in multiple myeloma cells receiving drugs over an extended period, suggesting a loss of centromere integrity.This research project will contribute to our understanding of epigenetic and transcriptional dynamics in MM. With our focus on the continuously changing abundance of transcription factors and co-regulators at promoters of cell cycle genes, we seek to unlock new pathways for molecular therapy, as well as identify more specific targets for treatment compared to blunt proteasome inhibition. Elucidating the mechanisms of action and resistance to proteasome inhibition will help advance future MM therapy. DisclosuresLulla:ASH Scholar Award: Research Funding; Leukemia Texas Research grant: Research Funding; Junior Faculty sees funding-Baylor College of Medicine: Research Funding; Lymphoma SPORE: Research Funding; ASBMT Young Investigator Award: Research Funding; Leukemia Texas: Membership on an entity's Board of Directors or advisory committees. Catic:Cancer Prevention and Research Institute of Texas: Research Funding; Ted Nash Long Life Foundation: Research Funding.

Haploid Bio-Induction in Plant through Mock Sexual Reproduction.

SummaryHaploidization is invaluable for basic genetic research and crop breeding. The haploid bio-induction principle is an important topic that remains largely unexplored. In this study, both CenH3 RNAi and in vitro inhibition were used to simulate and induce haploids in allopolyploid crop. Notably, in vitro CenH3 inhibition showed that the results were much the same to that of RNAi in phenotype, chromosome behavior, microspore production, and haploid induction. Cytological analyses of RNAi and inhibitor-treated progenies revealed elimination of chromosomes, defective microspores with empty nuclei, thereby giving rise to pseudo male gametes, and haploid parthenogenesis induction. We found distinct defective empty microspores that were positively correlated with the decrease of CenH3 during RNAi manipulation. Investigation through both in vivo and in vitro studies revealed that haploidization was induced through the pseudo male gamete-mediated mock sexual reproduction. The present results provide insights for the haploid parthenogenesis induction process.

Centromere deletion in Cryptococcus deuterogattii leads to neocentromere formation and chromosome fusions.

The human fungal pathogen Cryptococcus deuterogattii is RNAi-deficient and lacks active transposons in its genome. C. deuterogattii has regional centromeres that contain only transposon relics. To investigate the impact of centromere loss on the C. deuterogattii genome, either centromere 9 or 10 was deleted. Deletion of either centromere resulted in neocentromere formation and interestingly, the genes covered by these neocentromeres maintained wild-type expression levels. In contrast to cen9∆ mutants, cen10∆ mutant strains exhibited growth defects and were aneuploid for chromosome 10. At an elevated growth temperature (37°C), the cen10∆ chromosome was found to have undergone fusion with another native chromosome in some isolates and this fusion restored wild-type growth. Following chromosomal fusion, the neocentromere was inactivated, and the native centromere of the fused chromosome served as the active centromere. The neocentromere formation and chromosomal fusion events observed in this study in C. deuterogattii may be similar to events that triggered genomic changes within the Cryptococcus/Kwoniella species complex and may contribute to speciation throughout the eukaryotic domain.

Polyploidy and aneuploidy of seed plants from the Qinghai–Tibetan Plateau and their biological implications

The Qinghai–Tibetan Plateau is biologically diverse, with 9556 species of vascular plants in the 2,500,000 km2 plateau area. We focused on seed plants from the Qinghai–Tibetan Plateau. A total of 9321 species in the Qinghai–Tibetan Plateau were recorded. Sixty-one of these genera are Chinese endemics. Our results suggested that the flora of the Qinghai–Tibetan Plateau was characterized by relatively few polyploids, and aneuploidy was also considered as relatively rare. We inferred that aneuploidy may be affected by environmental factors and the addition or loss of centromeres. Furthermore, the highest frequency of polyploids was found among perennial herbs. Annuals had low polyploidy, and perennials had high polyploidy. Species richness was correlated with the incidence of polyploids, environmental conditions, and reproductive isolation.

DNA deletion as a mechanism for developmentally programmed centromere loss

A hallmark of active centromeres is the presence of the histone H3 variant CenH3 in the centromeric chromatin, which ensures faithful genome distribution at each cell division. A functional centromere can be inactivated, but the molecular mechanisms underlying the process of centromere inactivation remain largely unknown. Here, we describe the loss of CenH3 protein as part of a developmental program leading to the formation of the somatic nucleus in the eukaryote Paramecium. We identify two proteins whose depletion prevents developmental loss of CenH3: the domesticated transposase Pgm involved in the formation of DNA double strand cleavages and the Polycomb-like lysine methyltransferase Ezl1 necessary for trimethylation of histone H3 on lysine 9 and lysine 27. Taken together, our data support a model in which developmentally programmed centromere loss is caused by the elimination of DNA sequences associated with CenH3.

Acentric chromosome ends are prone to fusion with functional chromosome ends through a homology-directed rearrangement.

The centromeres of many eukaryotic chromosomes are established epigenetically on potentially variable tandem repeats; hence, these chromosomes are at risk of being acentric. We reported previously that artificially created acentric chromosomes in the fission yeast Schizosaccharomyces pombe can be rescued by end-to-end fusion with functional chromosomes. Here, we show that most acentric/functional chromosome fusion events in S. pombe cells harbouring an acentric chromosome I differed from the non-homologous end-joining-mediated rearrangements that result in deleterious dicentric fusions in normal cells, and were elicited by a previously unidentified homologous recombination (HR) event between chromosome end-associated sequences. The subtelomere repeats associated with the non-fusogenic ends were also destabilized in the surviving cells, suggesting a causal link between general subtelomere destabilization and acentric/functional chromosome fusion. A mutational analysis indicated that a non-canonical HR pathway was involved in the rearrangement. These findings are indicative of a latent mechanism that conditionally induces general subtelomere instability, presumably in the face of accidental centromere loss events, resulting in rescue of the fatal acentric chromosomes by interchromosomal HR.

Live and let die: centromere loss during evolution of plant chromosomes

SummaryFunctional centromeres, ensuring regular chromosome segregation in mitosis and meiosis, are a prerequisite for the evolutionary success of pre‐existing and new chromosome variants. The rapid progress in plant comparative genomics and cytogenetics brings new insights into the evolutionary fate of centromeres and mechanisms of chromosome number reduction (descending dysploidy). Centromere loss and relocation in chromosome regions with otherwise conserved collinearity can be explained by conventional mechanisms of chromosome rearrangements or, as newly available phylogenomic and cytogenomic data suggest, by centromere inactivation through epigenetic chromatin modifications and/or intra‐ and inter‐chromosomal recombination.

Loss of centromeric histone H3 (CENH3) from centromeres precedes uniparental chromosome elimination in interspecific barley hybrids

Uniparental chromosome elimination occurs in several interspecific hybrids of plants. We studied the mechanism underlying selective elimination of the paternal chromosomes during the early development of Hordeum vulgare × Hordeum bulbosum embryos. The following conclusions regarding the role of the centromere-specific histone H3 variant (CENH3) in the process of chromosome elimination were drawn: (i) centromere inactivity of H. bulbosum chromosomes triggers the mitosis-dependent process of uniparental chromosome elimination in unstable H. vulgare × H. bulbosum hybrids; (ii) centromeric loss of CENH3 protein rather than uniparental silencing of CENH3 genes causes centromere inactivity; (iii) in stable species combinations, cross-species incorporation of CENH3 occurs despite centromere-sequence differences, and not all CENH3 variants get incorporated into centromeres if multiple CENH3s are present in species combinations; and (iv) diploid barley species encode two CENH3 variants, the proteins of which are intermingled within centromeres throughout mitosis and meiosis.

New clues to understand how CENP-A maintains centromere identity

The centromere is a specialized chromosomal region that directs the formation of the kinetochore, a huge protein assembly that acts as the attachment site for spindle microtubules and carries out chromosome movement during cell division. Centromere loss or the presence of extra centromeres adversely affect chromosome segregation and may result in aneuploidy, a condition found in many human tumors and a major cause of miscarriages and birth defects. Consequently, understanding the basis of centromere determination and propagation is of great relevance to both fundamental and clinical research. In recent years, it has become clear that centromeres are defined by the presence of a histone H3 variant known as Centromere Protein A, CENP-A, or CenH3. Much effort has been devoted to understanding the mechanisms that drive the assembly of CENP-A containing nucleosomes exclusively onto centromeric DNA, as well as the peculiar structure of these nucleosomes. We have recently developed an immunofluorescence-based assay that measures CENP-A incorporation in the centromeres of chromosomes assembled in Xenopus egg extracts. The spatial and temporal specificity of CENP-A deposition observed in human cells can be recapitulated in this in vitro system, making it suitable to dissect the precise role of the different factors that contribute to this pathway. Here, we discuss our results together with other recent advances in our understanding of the mechanisms that mediate centromere inheritance.

Fast Diploidization in Close Mesopolyploid Relatives ofArabidopsis

Mesopolyploid whole-genome duplication (WGD) was revealed in the ancestry of Australian Brassicaceae species with diploid-like chromosome numbers (n = 4 to 6). Multicolor comparative chromosome painting was used to reconstruct complete cytogenetic maps of the cryptic ancient polyploids. Cytogenetic analysis showed that the karyotype of the Australian Camelineae species descended from the eight ancestral chromosomes (n = 8) through allopolyploid WGD followed by the extensive reduction of chromosome number. Nuclear and maternal gene phylogenies corroborated the hybrid origin of the mesotetraploid ancestor and suggest that the hybridization event occurred approximately 6 to 9 million years ago. The four, five, and six fusion chromosome pairs of the analyzed close relatives of Arabidopsis thaliana represent complex mosaics of duplicated ancestral genomic blocks reshuffled by numerous chromosome rearrangements. Unequal reciprocal translocations with or without preceeding pericentric inversions and purported end-to-end chromosome fusions accompanied by inactivation and/or loss of centromeres are hypothesized to be the main pathways for the observed chromosome number reduction. Our results underline the significance of multiple rounds of WGD in the angiosperm genome evolution and demonstrate that chromosome number per se is not a reliable indicator of ploidy level.

Centromere identity: a challenge to be faced

The centromere is a genetic locus, required for faithful chromosome segregation, where spindle fibers attach to the chromosome through kinetochore. Loss of centromere or formation of multiple centromeres on a single chromosome leads to chromosome missegregation or chromosome breakage, respectively, which are detrimental for fitness and survival of a cell. Therefore, understanding the mechanism of centromere locus determination on the chromosome and perpetuation of such a locus in subsequent generation (known as centromere identity) is very fundamental to combat conditions like aneuploidy, spontaneous abortion, developmental defects, cell lethality and cancer. Recent studies have come up with different models to explain centromere identity. However, the exact mechanism still remains elusive. It has been observed that most eukaryotic centromeres are determined epigenetically rather than by a DNA sequence. The epigenetic marks that are instrumental in determining centromere identity are the histone H3 variant, CENP-A and the specialized posttranslational modification of the core histones. Here we will review the recent studies on the factors responsible for generating unique centromeric chromatin and how it perpetuates during cell division giving the present-day models. We will further focus on the probable mechanism of de novo centromere formation with an example of neocentromere. As a matter of similitude, this review will include marking extrachromosomal chromatin to be served as a partitioning locus by deposition of CENP-A homolog in budding yeast.

Absence of ESR1 amplification in a series of breast cancers

Jos e Ad ela€ide, Pascal Finetti, Emmanuelle Charafe-Jauffret, Julien Wicinski, Jocelyne Jacquemier, Christos Sotiriou, Francois Bertucci, Daniel Birnbaum and Max Chaffanet* Centre de Recherche en Canc erologie de Marseille, UMR891 Inserm, Institut Paoli-Calmettes, 27 Bd. Le€i Roure, 13009 Marseille, France Functional Genomics & Translational Research Unit, Institut Jules Bordet, Boulevard de Waterloo, 125, B-1000 Brussels, Belgium

Centromeric loss in translocation of centric fusion type in cattle and water buffalo.

Iannuzzi, L., Di Berardino, D., Gustavsson, I., Ferrara, L. and Di Meo, G. P. 1987. Centromeric loss in translocations of centric fusion type in cattle and water buffalo. - Hereditas 106: 73–81. Lund, Sweden. ISSN 0018–0661. Received March 15, 1986 Robertsonian translocations in Podolian and Romagna cattle (Bos taurus L.) and Asiatic river buffaloes (Bubulus bubalis L.) were studied with C, G + C, and R-banding techniques. The investigation demonstrated: (a) presence of one block of constitutive heterochromatin in the q-arm of the cattle translocation chromosome; (b) chromosomes identified as 1 and 25 according to the system used - but presumptively 1 and 29 as earlier described - being involved in the cattle centric fusions, with the centromere region of chromosome 25(29) being lost and that of chromosome 1 being retained; (c) no constitutive heterochromatin in the q-chromosome arm of the bi-armed chromosomes 1 and 5 in the water huffaloes (with retention of the constitutive heterochromatin in their p-arms) and partial losses of centromeric heterochromatin in both arms of chromosomes 2, 3 and 4; (d) presence of a C-positive segment in the telomere region of the p-arm of chromosome 4 in the water buffalo; (e) no bi-armed chromosome common for the two species. Karyotype evolution is discussed and the urgency of an appropriate nomenclature system for cattle and buffalo chromosomes is briefly stressed.

DNA deformability changes of single base pair mutants within CDE binding sites in S. Cerevisiae centromere DNA correlate with measured chromosomal loss rates and CDE binding site symmetries

BackgroundThe centromeres in yeast (S. cerevisiae) are organized by short DNA sequences (125 bp) on each chromosome consisting of 2 conserved elements: CDEI and CDEIII spaced by a CDEII region. CDEI and CDEIII are critical sequence specific protein binding sites necessary for correct centromere formation and following assembly with proteins, are positioned near each other on a specialized nucleosome. Hegemann et al. BioEssays 1993, 15: 451–460 reported single base DNA mutants within the critical CDEI and CDEIII binding sites on the centromere of chromosome 6 and quantitated centromere loss of function, which they measured as loss rates for the different chromosome 6 mutants during cell division. Olson et al. Proc Natl Acad Sci USA 1998, 95: 11163–11168 reported the use of protein-DNA crystallography data to produce a DNA dinucleotide protein deformability energetic scale (PD-scale) that describes local DNA deformability by sequence specific binding proteins. We have used the PD-scale to investigate the DNA sequence dependence of the yeast chromosome 6 mutants' loss rate data. Each single base mutant changes 2 PD-scale values at that changed base position relative to the wild type. In this study, we have utilized these mutants to demonstrate a correlation between the change in DNA deformability of the CDEI and CDEIII core sites and the overall experimentally measured chromosome loss rates of the chromosome 6 mutants.ResultsIn the CDE I and CDEIII core binding regions an increase in the magnitude of change in deformability of chromosome 6 single base mutants with respect to the wild type correlates to an increase in the measured chromosome loss rate. These correlations were found to be significant relative to 105 Monte Carlo randomizations of the dinucleotide PD-scale applied to the same calculation. A net loss of deformability also tends to increase the loss rate. Binding site position specific, 4 data-point correlations were also created using the wild type sequence and the 3 associated alternate base mutants at each binding site position. These position specific slope magnitudes, or sensitivities, correlated with and reflected the underlying position symmetry of the DNA binding sequences.ConclusionThese results suggest the utility of correlating quantitative aspects of sequence specific protein-DNA complex single base mutants with changes in the easily calculated PD-deformability scale of the individual DNA sequence mutants. Using this PD approach, it may be possible in the future to understand the magnitude of biological or energetic functional effects of specific DNA sequence mutants within DNA-protein complexes in terms of their effect on DNA deformability.

Chromosomal localization of conglutinin (CGN1) gene to river buffalo by sequential RBH-banding and FISH.

Chromosomal localization of conglutinin (CGN1) gene to river buffalo by sequential RBH-banding and FISH.

Detection of numerical chromosome anomalies in interphase cells of ovarian carcinomas using fluorescence in situ hybridization.

Fluorescence in situ hybridization was used in interphase cells of 30 ovarian carcinomas to detect numerical changes in copy number of 13 different centromeres (1, 2, 3, 4, 6, 7, 8, 10, 11, 12, 17, 18, and X). Thirty-seven percent of samples (11/30) were near diploid and demonstrated only minor changes in centromere copy number, involving gain and/or loss of one or a few centromeres. The most common changes included loss of centromeres 4,6, 17, and 18 and gain of centromere 1. The remaining 63% of samples were hyperdiploid and demonstrated a general increase in copy number of most or all centromeres examined. Among these samples, the centromere of chromosome I was most often found to be at higher copy number. Centromeres that were less often at increased copy or deleted within the hyperdiploid samples include centromeres 4, 17, 18, and X. These results suggest that tumor-suppressor genes that are located on chromosomes 4, 6, 17, and 18 may be involved in the development and progression of ovarian cancer.

Some preliminary cytological observations on a new basic number in Paspalum convexum (Gramineae)

That Paspalum convexum Humb. and Bonpl. is a valid member of the Plicatula species complex has been substantiated morphologically and anatomically, but its chromosome complement of n = 16 is very different. Four of its 16 bivalent chromosomes are larger than the others and are not quadrivalent associations, as had been suspected previously. With evidence that 10 is the basic number for the group, as well as for the genus as a whole, several mechanisms are proposed that would increase or reduce x = 10 or its multiple to a basic complement of 16 through gain or loss of centromeres, respectively.

Cytogenetics and evolution ofMatricaria and related genera (asteraceae-anthemideae)

1. Chromosome numbers resp. karyotypes are established and compared for 18 species of the Anthemideae generaAnthemis, Chamaemelum, Tripleurospermum, Matricaria, Sphaeroclinium, andPentzia (Table 1, Figs. 1–2). 2. Selfing tests demonstrate that various perennial and annual species of these genera are predominantly selfsterile; onlyMatricaria discoidea is an obligate inbreeder (p. 162f.). 3. An experimental crossing programm involving 12 species from 5 genera has resulted in 22 successful F1-combinations which where analysed in regard to morphology, chromosome number, pollen meiotic behaviour, pollen (and partly seed) fertility (Fig. 3), and compared with their parents (Figs. 4–18, Tables 3–17). 4. Karyotype similarities, F1-chromosome pairing and F1-fertility together with morphological, embryological, biochemical and other data contribute to the controversial problem of relationships and systematics of Anthemideae (p. 183–188):Anthemis is rather heterogeneous, its subgen.Cota may deserve generic status, sect.Maruta approachesChamaemelum; Tripleurospermum is coherent; the two latter genera linkAnthemis with the more advancedMatricaria; they all form a related N. Hemisphere group. S. Hemisphere taxa are more remote: “Matricaria” nigellifolia is much closer toCotula and should be placed in the genusSphaeroclinium; the inclusion of other “Matricariae” into the S. African genusPentzia is justified; some form the hitherto unrecognized annualP. globifera group. 5. Cytogenetic results illustrate mechanisms underlying evolutionary differentiation of Anthemideae (p. 188–194): genie and cytoplasmic factors determine color and shape of flowers, presence or absence of paleae, azulene content, etc.; small karyotype changes appear already within species and gradually reduce chromosome pairing affinities in species hybrids; gross translocations and loss of centromeres have led to species divergence and descending dysploidy (2 n=16→12) in thePentzia globifera group; experimental allotetraploids have originated from intergeneric hybridization involving 2x members ofAnthemis, Tripleurospermum, andMatricaria; through unreduced gametes several 3x progenies have been produced; reproductive barriers between species and genera are of very complex nature. Different recombination systems and evolutionary strategies within Anthemideae are discussed (p. 194f.).