scholarly journals Recurrent losses and rapid evolution of the condensin II complex in insectsg

2018 ◽  
Author(s):  
T. King ◽  
C.J. Leonard ◽  
J.C. Cooper ◽  
S. Nguyen ◽  
E. Joyce ◽  
...  
Keyword(s):  
Genome Organization ◽  
Molecular Mechanisms ◽  
Somatic Cells ◽  
Rapid Evolution ◽  
Genetic Material ◽  
Life Forms ◽  
Model Organisms ◽  
Homologous Chromosomes ◽  
Homologous Chromosome Pairing ◽  
Key Aspects

AbstractCondensins play a crucial role in the organization of genetic material by compacting and disentangling chromosomes. The condensin I and condensin II complexes are widely considered to have distinct functions based on studies in a few model organisms, although the specific functions of each complex are yet to be fully understood. The condensin II complex is critical for genome organization in Drosophila, and is a key anti-pairing factor that separates homologous chromosomes in somatic cells. Intriguingly, the Cap-G2 subunit of condensin II is absent in Drosophila melanogaster, and this loss may be related to the high levels of homologous chromosome pairing in somatic cells seen in flies. Here, we find that this Cap-G2 loss predates the origin of Dipterans, and other CapG2 losses have occurred independently in multiple insect lineages. Furthermore, the Cap-H2 and Cap-D3 subunits have also been repeatedly and independently lost in several insect orders, and some taxa lack condensin II-specific subunits entirely. We used Oligopaint DNA-FISH to quantify pairing levels in ten species across seven orders, representing several different configurations of the condensin II complex. We find that all non-Dipteran insects display near-uniform low pairing levels, suggesting that some key aspects of genome organization are robust to condensin II subunit losses. Finally, we observe consistent signatures of positive selection in condensin II subunits across flies and mammals. These findings suggest that these ancient complexes are far more evolutionarily labile than previously suspected, and are at the crossroads of several forms of genomic conflicts. Our results raise fundamental questions about the specific functions of the two condensin complexes and the interplay between them in taxa that have experienced subunit losses, and open the door to further investigations to elucidate the diversity of molecular mechanisms that underlie genome organization across various life forms.

scholarly journals Recurrent Losses and Rapid Evolution of the Condensin II Complex in Insects

2019 ◽  
Vol 36 (10) ◽  
pp. 2195-2204 ◽  
Author(s):  
Thomas D King ◽  
Christopher J Leonard ◽  
Jacob C Cooper ◽  
Son Nguyen ◽  
Eric F Joyce ◽  
...  
Keyword(s):  
Genome Organization ◽  
Molecular Mechanisms ◽  
Rapid Evolution ◽  
Genetic Material ◽  
Life Forms ◽  
Model Organisms ◽  
Complex Composition ◽  
Homologous Chromosomes ◽  
Somatic Pairing ◽  
Key Aspects

Abstract Condensins play a crucial role in the organization of genetic material by compacting and disentangling chromosomes. Based on studies in a few model organisms, the condensins I and II complexes are considered to have distinct functions, with the condensin II complex playing a role in meiosis and somatic pairing of homologous chromosomes in Drosophila. Intriguingly, the Cap-G2 subunit of condensin II is absent in Drosophila melanogaster, and this loss may be related to the high levels of chromosome pairing seen in flies. Here, we find that all three non-SMC subunits of condensin II (Cap-G2, Cap-D3, and Cap-H2) have been repeatedly and independently lost in taxa representing multiple insect orders, with some taxa lacking all three. We also find that all non-Dipteran insects display near-uniform low-pairing levels regardless of their condensin II complex composition, suggesting that some key aspects of genome organization are robust to condensin II subunit losses. Finally, we observe consistent signatures of positive selection in condensin subunits across flies and mammals. These findings suggest that these ancient complexes are far more evolutionarily labile than previously suspected, and are at the crossroads of several forms of genomic conflicts. Our results raise fundamental questions about the specific functions of the two condensin complexes in taxa that have experienced subunit losses, and open the door to further investigations to elucidate the diversity of molecular mechanisms that underlie genome organization across various life forms.

scholarly journals DNA Damaged Induced Cell Death in Oocytes

Molecules ◽  
2020 ◽  
Vol 25 (23) ◽  
pp. 5714
Author(s):  
Jakob Gebel ◽  
Marcel Tuppi ◽  
Nicole Sänger ◽  
Björn Schumacher ◽  
Volker Dötsch
Keyword(s):  
Quality Control ◽  
Control System ◽  
Molecular Mechanisms ◽  
P53 Protein ◽  
Genetic Material ◽  
Fruit Fly ◽  
Quality Control System ◽  
Premature Menopause ◽  
Dna Double Strand Breaks ◽  
Homologous Chromosomes

The production of haploid gametes through meiosis is central to the principle of sexual reproduction. The genetic diversity is further enhanced by exchange of genetic material between homologous chromosomes by the crossover mechanism. This mechanism not only requires correct pairing of homologous chromosomes but also efficient repair of the induced DNA double-strand breaks. Oocytes have evolved a unique quality control system that eliminates cells if chromosomes do not correctly align or if DNA repair is not possible. Central to this monitoring system that is conserved from nematodes and fruit fly to humans is the p53 protein family, and in vertebrates in particular p63. In mammals, oocytes are stored for a long time in the prophase of meiosis I which, in humans, can last more than 50 years. During the entire time of this arrest phase, the DNA damage checkpoint remains active. The treatment of female cancer patients with DNA damaging irradiation or chemotherapeutics activates this checkpoint and results in elimination of the oocyte pool causing premature menopause and infertility. Here, we review the molecular mechanisms of this quality control system and discuss potential therapeutic intervention for the preservation of the oocyte pool during chemotherapy.

The origin of sex and the nature of species

1997 ◽  
Author(s):  
John Maynard Smith ◽  
Eors Szathmary
Keyword(s):  
Molecular Mechanisms ◽  
Genetic Material ◽  
Metabolic Efficiency ◽  
Recombinational Repair ◽  
Cellular Mechanisms ◽  
Homologous Chromosomes ◽  
Sexual Recombination ◽  
One Step ◽  
Regular Succession ◽  
Two Phases

By sex in eukaryotes, we understand a more-or-less regular succession of meiosis and syngamy. A natural consequence of this is the alternation of haploid and diploid phases in the life cycle. Eukaryotic sex significantly differs from prokaryotic sex in two crucial respects: the cellular mechanisms are quite different, and the transfer of genetic material in prokaryotes is less frequent and more localized (Maynard Smith et al., 1991). However, there seems to be significant continuity in the molecular mechanisms: sex in either case requires recombination enzymes, many of which are active in repair of damaged DNA as well. Thus, it seems plausible that recombinational repair was a preadaptation for sexual recombination. We mention in passing that there is a theory that selection for the recombinational repair of doublestrand DNA damage is responsible for the current maintenance of eukaryotic sex (Bernstein et al., 1981, 1988), but there are severe theoretical as well as factual problems with this theory; we will mention some factual difficulties later. Although an alternation of haploid and diploid phases follows from sex, a clue to the origin problem may lie in the idea that this alternation existed before the evolution of sexual recombination proper. The first hint that this may have been so comes from the classic paper by Cleveland (1947), where he proposed that the haploid-diploid cycle may have started with a spontaneous diploidization by endomitosis: that is, without syngamy. His suggestions were based on original observations on primitive flagellates (hypermastigotes and polymastigotes). Among them, Barbulanympha has a regular endomitosis-meiosis cycle. Margulis & Sagan (1986) called renewed attention to Cleveland’s ideas. In particular, they argued that the alternation of ploidy phases could have a primarily ecological explanation: if the environment alternates in some important factors, this may drive a haploid-diploid cycle, provided the phases are adaptations to different environments. For example, diploids have a smaller relative surface area than haploids, which may confer higher metabolic efficiency. We shall come back to such ideas soon. We focus first on the possible cellular mechanisms connecting the two phases. It is important that some protists have a one-step rather than a two-step meiosis: after syngamy, the two homologous chromosomes become disjunct without premeiotic doubling.

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

Nature ◽  
2021 ◽  
Author(s):  
Fides Zenk ◽  
Yinxiu Zhan ◽  
Pavel Kos ◽  
Eva Löser ◽  
Nazerke Atinbayeva ◽  
...  
Keyword(s):  
Genome Organization ◽  
Molecular Mechanisms ◽  
High Throughput Sequencing ◽  
De Novo ◽  
Early Embryo ◽  
Heterochromatin Protein ◽  
Chromosome Conformation ◽  
3D Genome ◽  
Genome Reorganization

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

scholarly journals Pathophysiology of Atherosclerotic Plaque Development-Contemporary Experience and New Directions in Research

2021 ◽  
Vol 22 (7) ◽  
pp. 3513
Author(s):  
Michal Kowara ◽  
Agnieszka Cudnoch-Jedrzejewska
Keyword(s):  
Atherosclerotic Plaque ◽  
Molecular Mechanisms ◽  
Cellular Heterogeneity ◽  
Ldl Oxidation ◽  
Plaque Development ◽  
New Directions ◽  
Life Threatening ◽  
Non Coding Rnas ◽  
Cellular Pathways ◽  
Key Aspects

Atherosclerotic plaque is the pathophysiological basis of important and life-threatening diseases such as myocardial infarction. Although key aspects of the process of atherosclerotic plaque development and progression such as local inflammation, LDL oxidation, macrophage activation, and necrotic core formation have already been discovered, many molecular mechanisms affecting this process are still to be revealed. This minireview aims to describe the current directions in research on atherogenesis and to summarize selected studies published in recent years—in particular, studies on novel cellular pathways, epigenetic regulations, the influence of hemodynamic parameters, as well as tissue and microorganism (microbiome) influence on atherosclerotic plaque development. Finally, some new and interesting ideas are proposed (immune cellular heterogeneity, non-coding RNAs, and immunometabolism) which will hopefully bring new discoveries in this area of investigation.

scholarly journals Rapid evolution and molecular convergence in cryptorchidism-related genes associated with inherently undescended testes in mammals

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Simin Chai ◽  
Ran Tian ◽  
Juanjuan Bi ◽  
Shixia Xu ◽  
Guang Yang ◽  
...  
Keyword(s):  
Muscle Development ◽  
Rapid Evolution ◽  
Genetic Material ◽  
Comparative Genomic ◽  
Testicular Descent ◽  
Ancestral State ◽  
Undescended Testes ◽  
Genomic Analyses ◽  
Genetic Mechanisms ◽  
Molecular Convergence

Abstract Background The mammalian testis is an important male exocrine gland and spermatozoa-producing organ that usually lies in extra-abdominal scrotums to provide a cooler environment for spermatogenesis and sperm storage. Testicles sometimes fail to descend, leading to cryptorchidism. However, certain groups of mammals possess inherently ascrotal testes (i.e. testes that do not descend completely or at all) that have the same physiological functions as completely descended scrotal testes. Although several anatomical and hormonal factors involved in testicular descent have been studied, there is still a paucity of comprehensive research on the genetic mechanisms underlying the evolution of testicular descent in mammals and how mammals with ascrotal testes maintain their reproductive health. Results We performed integrative phenotypic and comparative genomic analyses of 380 cryptorchidism-related genes and found that the mammalian ascrotal testes trait is derived from an ancestral scrotal state. Rapidly evolving genes in ascrotal mammals were enriched in the Hedgehog pathway—which regulates Leydig cell differentiation and testosterone secretion—and muscle development. Moreover, some cryptorchidism-related genes in ascrotal mammals had undergone positive selection and contained specific mutations and indels. Genes harboring convergent/parallel amino acid substitutions between ascrotal mammals were enriched in GTPase functions. Conclusions Our results suggest that the scrotal testis is an ancestral state in mammals, and the ascrotal phenotype was derived multiple times in independent lineages. In addition, the adaptive evolution of genes involved in testicular descent and the development of the gubernaculum contributed to the evolution of ascrotal testes. Accurate DNA replication, the proper segregation of genetic material, and appropriate autophagy are the potential mechanisms for maintaining physiological normality during spermatogenesis in ascrotal mammals. Furthermore, the molecular convergence of GTPases is probably a mechanism in the ascrotal testes of different mammals. This study provides novel insights into the evolution of the testis and scrotum in mammals and contributes to a better understanding of the pathogenesis of cryptorchidism in humans.

Microglia extracellular vesicles: focus on molecular composition and biological function

2021 ◽  
Vol 49 (4) ◽  
pp. 1779-1790 ◽  
Author(s):  
Lorenzo Ceccarelli ◽  
Chiara Giacomelli ◽  
Laura Marchetti ◽  
Claudia Martini
Keyword(s):  
Extracellular Vesicles ◽  
Molecular Mechanisms ◽  
Biological Function ◽  
Biological Effects ◽  
Genetic Material ◽  
Cell Communication ◽  
Molecular Composition ◽  
Cargo Proteins ◽  
A Cell ◽  
The Central Nervous System

Extracellular vesicles (EVs) are a heterogeneous family of cell-derived lipid bounded vesicles comprising exosomes and microvesicles. They are potentially produced by all types of cells and are used as a cell-to-cell communication method that allows protein, lipid, and genetic material exchange. Microglia cells produce a large number of EVs both in resting and activated conditions, in the latter case changing their production and related biological effects. Several actions of microglia in the central nervous system are ascribed to EVs, but the molecular mechanisms by which each effect occurs are still largely unknown. Conflicting functions have been ascribed to microglia-derived EVs starting from the neuronal support and ending with the propagation of inflammation and neurodegeneration, confirming the crucial role of these organelles in tuning brain homeostasis. Despite the increasing number of studies reported on microglia-EVs, there is also a lot of fragmentation in the knowledge on the mechanism at the basis of their production and modification of their cargo. In this review, a collection of literature data about the surface and cargo proteins and lipids as well as the miRNA content of EVs produced by microglial cells has been reported. A special highlight was given to the works in which the EV molecular composition is linked to a precise biological function.

scholarly journals Mitotic antipairing of homologous and sex chromosomes via spatial restriction of two haploid sets

2018 ◽  
Vol 115 (52) ◽  
pp. E12235-E12244 ◽  
Author(s):  
Lisa L. Hua ◽  
Takashi Mikawa
Keyword(s):  
Genome Instability ◽  
Cell Types ◽  
Parental Origin ◽  
Meridional Plane ◽  
Homologous Chromosomes ◽  
Daughter Cells ◽  
Homologous Chromosome Pairing ◽  
Multiple Cell ◽  
Mouse Cells ◽  
Nuclear Polarity

Pairing homologous chromosomes is required for recombination. However, in nonmeiotic stages it can lead to detrimental consequences, such as allelic misregulation and genome instability, and is rare in human somatic cells. How mitotic recombination is prevented—and how genetic stability is maintained across daughter cells—is a fundamental, unanswered question. Here, we report that both human and mouse cells impede homologous chromosome pairing by keeping two haploid chromosome sets apart throughout mitosis. Four-dimensional analysis of chromosomes during cell division revealed that a haploid chromosome set resides on either side of a meridional plane, crossing two centrosomes. Simultaneous tracking of chromosome oscillation and the spindle axis, using fluorescent CENP-A and centrin1, respectively, demonstrates collective genome behavior/segregation of two haploid sets throughout mitosis. Using 3D chromosome imaging of a translocation mouse with a supernumerary chromosome, we found that this maternally derived chromosome is positioned by parental origin. These data, taken together, support the identity of haploid sets by parental origin. This haploid set-based antipairing motif is shared by multiple cell types, doubles in tetraploid cells, and is lost in a carcinoma cell line. The data support a mechanism of nuclear polarity that sequesters two haploid sets along a subcellular axis. This topological segregation of haploid sets revisits an old model/paradigm and provides implications for maintaining mitotic fidelity.

Insights into the seasonal adaptive mechanisms of Chinese alligators (Alligator sinensis) from transcriptomic analyses

2018 ◽  
Vol 66 (2) ◽  
pp. 93 ◽  
Author(s):  
Hongji Sun ◽  
Xianbo Zuo ◽  
Long Sun ◽  
Peng Yan ◽  
Fang Zhang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Molecular Mechanisms ◽  
Differentially Expressed ◽  
Model Organisms ◽  
Seasonal Adaptation ◽  
Cold Temperatures ◽  
Chinese Alligator ◽  
Adaptive Mechanisms ◽  
Alligator Sinensis

The Chinese alligator (Alligator sinensis) is an endemic and rare species in China, and is considered to be one of the most endangered vertebrates in the world. It is known to hibernate, an energy-saving strategy against cold temperatures and food deprivation. Changes in gene expression during hibernation remain largely unknown. To understand these complex seasonal adaptive mechanisms, we performed a comprehensive survey of differential gene expression in heart, skeletal muscle, and kidney of hibernating and active Chinese alligators using RNA-Sequencing. In total, we identified 4780 genes differentially expressed between the active and hibernating periods. GO and KEGG pathway analysis indicated the likely role of these differentially expressed genes (DEGs). The upregulated DEGs in the active Chinese alligator, CSRP3, MYG and PCKGC, may maintain heart and skeletal muscle contraction, transport and storage of oxygen, and enhance the body’s metabolism, respectively. The upregulated DEGs in the dormant Chinese alligator, ADIPO, CIRBP and TMM27, may improve insulin sensitivity and glucose/lipid metabolism, protect cells against harmful effects of cold temperature and hypoxia, regulate amino acid transport and uptake, and stimulate the proliferation of islet cells and the secretion of insulin. These results provide a foundation for understanding the molecular mechanisms of the seasonal adaptation required for hibernation in Chinese alligators, as well as effective information for other non-model organisms research.

scholarly journals How Can Satellite DNA Divergence Cause Reproductive Isolation? Let Us Count the Chromosomal Ways

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Patrick M. Ferree ◽  
Satyaki Prasad
Keyword(s):  
Reproductive Isolation ◽  
Developmental Stages ◽  
Rapid Evolution ◽  
Model Organisms ◽  
Cellular Mechanisms ◽  
Closely Related Species ◽  
Heterochromatin Formation ◽  
Interspecies Hybrids ◽  
Postzygotic Reproductive Isolation ◽  
And Function

Satellites are one of the most enigmatic parts of the eukaryotic genome. These highly repetitive, noncoding sequences make up as much as half or more of the genomic content and are known to play essential roles in chromosome segregation during meiosis and mitosis, yet they evolve rapidly between closely related species. Research over the last several decades has revealed that satellite divergence can serve as a formidable reproductive barrier between sibling species. Here we highlight several key studies on Drosophila and other model organisms demonstrating deleterious effects of satellites and their rapid evolution on the structure and function of chromosomes in interspecies hybrids. These studies demonstrate that satellites can impact chromosomes at a number of different developmental stages and through distinct cellular mechanisms, including heterochromatin formation. These findings have important implications for how loci that cause postzygotic reproductive isolation are viewed.

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