scholarly journals Live imaging and biophysical modeling support a button-based mechanism of somatic homolog pairing in Drosophila

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Myron Barber Child ◽  
Jack R Bateman ◽  
Amir Jahangiri ◽  
Armando Reimer ◽  
Nicholas C Lammers ◽  
...  
Keyword(s):  
Live Imaging ◽  
Biophysical Model ◽  
Structural Basis ◽  
Biophysical Modeling ◽  
Homologous Chromosomes ◽  
Homolog Pairing ◽  
Molecular Identity ◽  
Rna Labeling ◽  
Model Predictions ◽  
Chromosomal Loci

3D eukaryotic genome organization provides the structural basis for gene regulation. In Drosophila melanogaster, genome folding is characterized by somatic homolog pairing, where homologous chromosomes are intimately paired from end to end; however, how homologs identify one another and pair has remained mysterious. Recently, this process has been proposed to be driven by specifically interacting 'buttons' encoded along chromosomes. Here, we turned this hypothesis into a quantitative biophysical model to demonstrate that a button-based mechanism can lead to chromosome-wide pairing. We tested our model using live-imaging measurements of chromosomal loci tagged with the MS2 and PP7 nascent RNA labeling systems. We show solid agreement between model predictions and experiments in the pairing dynamics of individual homologous loci. Our results strongly support a button-based mechanism of somatic homolog pairing in Drosophila and provide a theoretical framework for revealing the molecular identity and regulation of buttons.

scholarly journals Live imaging and biophysical modeling support a button-based mechanism of somatic homolog pairing in Drosophila

2020 ◽  
Author(s):  
Myron Child ◽  
Jack R. Bateman ◽  
Amir Jahangiri ◽  
Armando Reimer ◽  
Nicholas C. Lammers ◽  
...  
Keyword(s):  
Spatial Configuration ◽  
Live Imaging ◽  
Biophysical Model ◽  
Structural Basis ◽  
Biophysical Modeling ◽  
Homologous Chromosomes ◽  
3D Genome ◽  
Homolog Pairing ◽  
Rna Labeling ◽  
Regulated Gene Expression

AbstractThe spatial configuration of the eukaryotic genome is organized and dynamic, providing the structural basis for regulated gene expression in living cells. In Drosophila melanogaster, 3D genome organization is characterized by somatic homolog pairing, where homologous chromosomes are intimately paired from end to end; however, the process by which homologs identify one another and pair has remained mysterious. A recent model proposed that specifically interacting “buttons” encoded along the lengths of homologous chromosomes drive somatic homolog pairing. Here, we turned this hypothesis into a precise biophysical model to demonstrate that a button-based mechanism can lead to chromosome-wide pairing. We tested our model and constrained its free parameters using live-imaging measurements of chromosomal loci tagged with the MS2 and PP7 nascent RNA labeling systems. Our analysis showed strong agreement between model predictions and experiments in the separation dynamics of tagged homologous loci as they transition from unpaired to paired states, and in the percentage of nuclei that become paired as embryonic development proceeds. In sum, as a result of this dialogue between theory and experiment, our data strongly support a button-based mechanism of somatic homolog pairing in Drosophila and provide a theoretical framework for revealing the molecular identity and regulation of buttons.

scholarly journals HOP1: a yeast meiotic pairing gene.

Genetics ◽  
1989 ◽  
Vol 121 (3) ◽  
pp. 445-462 ◽  
Author(s):  
N M Hollingsworth ◽  
B Byers
Keyword(s):  
Synaptonemal Complex ◽  
Structural Basis ◽  
Recessive Mutation ◽  
Intragenic Recombination ◽  
Meiotic Pairing ◽  
Homologous Chromosomes ◽  
Homolog Pairing ◽  
Chromosomal Pairing ◽  
Chromosome Iii ◽  
Cloned Gene

Abstract The recessive mutation, hop1-1, was isolated by use of a screen designed to detect mutations defective in homologous chromosomal pairing during meiosis in Saccharomyces cerevisiae. Mutants in HOP1 displayed decreased levels of meiotic crossing over and intragenic recombination between markers on homologous chromosomes. In contrast, assays of the hop1-1 mutation in a spo13-1 haploid disomic for chromosome III demonstrated that intrachromosomal recombination between directly duplicated sequences was unaffected. The spores produced by SPO13 diploids homozygous for hop1 were largely inviable, as expected for a defect in interhomolog recombination that results in high levels of nondisjunction. HOP1 was cloned by complementation of the spore lethality phenotype and the cloned gene was used to map HOP1 to the LYS11-HIS6 interval on the left arm of chromosome IX. Electron microscopy revealed that diploids homozygous for hop1 fail to form synaptonemal complex, which normally provides the structural basis for homolog pairing. We propose that HOP1 acts in meiosis primarily to promote chromosomal pairing, perhaps by encoding a component of the synaptonemal complex.

scholarly journals Potential for rapid genetic adaptation to warming in a Great Barrier Reef coral

2017 ◽  
Author(s):  
Mikhail V. Matz ◽  
Eric A. Treml ◽  
Galina V. Aglyamova ◽  
Madeleine J. H. van Oppen ◽  
Line K. Bay
Keyword(s):  
Genetic Variation ◽  
Great Barrier Reef ◽  
Coral Cover ◽  
Reef Coral ◽  
Biophysical Model ◽  
Detectable Effect ◽  
Genetic Adaptation ◽  
Barrier Reef ◽  
Biophysical Modeling ◽  
Adaptive Genetic Variation

AbstractCan genetic adaptation in reef-building corals keep pace with the current rate of sea surface warming? Here we combine population genomic, biophysical modeling, and evolutionary simulations to predict future adaptation of the common coralAcropora milleporaon the Great Barrier Reef. Loss of coral cover in recent decades did not yet have detectable effect on genetic diversity in our species. Genomic analysis of migration patterns closely matched the biophysical model of larval dispersal in favoring the spread of existing heat-tolerant alleles from lower to higher latitudes. Given these conditions we find that standing genetic variation could be sufficient to fuel rapid adaptation ofA. milleporato warming for the next 100-200 years, although random thermal anomalies would drive increasingly severe mortality episodes. However, this adaptation will inevitably cease unless the warming is slowed down, since no realistic mutation rate could replenish adaptive genetic variation fast enough.

scholarly journals Lobster Fishery Connectivity and Management in Indonesia Waters

2021 ◽  
Vol 3 (1) ◽  
Author(s):  
Waluyo Waluyo ◽  
Taslim Arifin
Keyword(s):  
Genetic Structure ◽  
Fishery Management ◽  
Marine Organism ◽  
Molecular Genetic ◽  
Three Dimensional ◽  
Geographical Information ◽  
Biophysical Model ◽  
Complex Life Cycle ◽  
Biophysical Modeling ◽  
The Individual

The distribution of lobsters in Indonesia waters is very wide, even lobster species in Indonesia are also scattered in the tropical waters of the western Pacific Ocean, the Indian Ocean, Africa to Japanese waters.Indonesia waters are divided into 11 (eleven) Fishery Management Zone (FMZ). Lobsters in Indonesia may come from various water areas, both national and regional waters zone, it’s called the sink population, its spread is influenced by the movement of the current. Lobster seed is nurtured by nature through oceancurrents from Australia, East Indonesia, Japan, then back to Australia. Lobsters have a complex life cycle,where adult lobsters inhabit coral reefs as a place to lay eggs, then hatch into planktonic larvae, and grow up in open seas and carry out diurnal and ontogenetic vertical migrations before returning to nurseries in shallow coastal areas and reefs. coral, as well as habitat by the type of species. Literature research had used at leasttwo methodologies to estimate the distribution and connection sensitivity matrices of marine organism larvae.The two most common approaches are using genetic markers and numerical biophysical modeling. Thus, this research uses molecular genetic techniques to explain the genetic structure of lobster populations using a biophysical model approach that can explain the genetic structure of lobsters, as well as the distribution base on regional oceanographic synthesis data and lobster biology known in Indonesia waters. This model has four components, namely: 1) a benthic module based on a Geographical Information System (GIS) which is a lobster habitat in the spawning and recruitment process, 2) a physical oceanography module containing daily velocity in the form of a three-dimensional hydrodynamic model, 3) a larva biology module that describes larval life history characteristics, and 4) a Lagrangian Stochastic module that tracks the individual trajectories of larvae.

scholarly journals Three-dimensional Ultrastructure of Saccharomyces cerevisiae Meiotic Spindles

2005 ◽  
Vol 16 (3) ◽  
pp. 1178-1188 ◽  
Author(s):  
Mark Winey ◽  
Garry P. Morgan ◽  
Paul D. Straight ◽  
Thomas H. Giddings ◽  
David N. Mastronarde
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Meiotic Chromosome ◽  
Three Dimensional ◽  
Structural Basis ◽  
Mitotic Spindles ◽  
Yeast Saccharomyces Cerevisiae ◽  
Homologous Chromosomes ◽  
Sister Chromatids ◽  
Single Nucleus ◽  
Meiotic Spindles

Meiotic chromosome segregation leads to the production of haploid germ cells. During meiosis I (MI), the paired homologous chromosomes are separated. Meiosis II (MII) segregation leads to the separation of paired sister chromatids. In the budding yeast Saccharomyces cerevisiae, both of these divisions take place in a single nucleus, giving rise to the four-spored ascus. We have modeled the microtubules in 20 MI and 15 MII spindles by using reconstruction from electron micrographs of serially sectioned meiotic cells. Meiotic spindles contain more microtubules than their mitotic counterparts, with the highest number in MI spindles. It is possible to differentiate between MI versus MII spindles based on microtubule numbers and organization. Similar to mitotic spindles, kinetochores in either MI or MII are attached by a single microtubule. The models indicate that the kinetochores of paired homologous chromosomes in MI or sister chromatids in MII are separated at metaphase, similar to mitotic cells. Examination of both MI and MII spindles reveals that anaphase A likely occurs in addition to anaphase B and that these movements are concurrent. This analysis offers a structural basis for considering meiotic segregation in yeast and for the analysis of mutants defective in this process.

scholarly journals The Zebrafish Meiotic Cohesin Complex Protein Smc1b Is Required for Key Events in Meiotic Prophase I

2021 ◽  
Vol 9 ◽  
Author(s):  
Kazi Nazrul Islam ◽  
Maitri Mitesh Modi ◽  
Kellee Renee Siegfried
Keyword(s):  
Essential Role ◽  
Cohesin Complex ◽  
Dna Double Strand Breaks ◽  
Homologous Chromosomes ◽  
Homolog Pairing ◽  
Complex Protein ◽  
Complete Failure ◽  
Cell Arrest ◽  
Key Events

The eukaryotic structural maintenance of chromosomes (SMC) proteins are involved in key processes of chromosome structure and dynamics. SMC1β was identified as a component of the meiotic cohesin complex in vertebrates, which aids in keeping sister chromatids together prior to segregation in meiosis II and is involved in association of homologous chromosomes in meiosis I. The role of SMC1β in meiosis has primarily been studied in mice, where mutant male and female mice are infertile due to germ cell arrest at pachytene and metaphase II stages, respectively. Here, we investigate the function of zebrafish Smc1b to understand the role of this protein more broadly in vertebrates. We found that zebrafish smc1b is necessary for fertility and has important roles in meiosis, yet has no other apparent roles in development. Therefore, smc1b functions primarily in meiosis in both fish and mammals. In zebrafish, we showed that smc1b mutant spermatocytes initiated telomere clustering in leptotene, but failed to complete this process and progress into zygotene. Furthermore, mutant spermatocytes displayed a complete failure of synapsis between homologous chromosomes and homolog pairing only occurred at chromosome ends. Interestingly, meiotic DNA double strand breaks occurred in the absence of Smc1b despite failed pairing and synapsis. Overall, our findings point to an essential role of Smc1b in the leptotene to zygotene transition during zebrafish spermatogenesis. In addition, ovarian follicles failed to form in smc1b mutants, suggesting an essential role in female meiosis as well. Our results indicate that there are some key differences in Smc1b requirement in meiosis among vertebrates: while Smc1b is not required for homolog pairing and synapsis in mice, it is essential for these processes in zebrafish.

scholarly journals Time-course analysis of early meiotic prophase events informs mechanisms of homolog pairing and synapsis in Caenorhabditis elegans

2017 ◽  
Author(s):  
Susanna Mlynarczyk-Evans ◽  
Anne M Villeneuve
Keyword(s):  
Caenorhabditis Elegans ◽  
Meiotic Prophase ◽  
Time Course ◽  
S Phase ◽  
Resolution Time ◽  
X Chromosomes ◽  
Homologous Chromosomes ◽  
Homolog Pairing ◽  
Nuclear Reorganization ◽  
Active Mobilization

AbstractSegregation of homologous chromosomes during meiosis depends on their ability to reorganize within the nucleus, discriminate among potential partners, and stabilize pairwise associations through assembly of the synaptonemal complex (SC). Here we report a high-resolution time-course analysis of these key early events during Caenorhabditis elegans meiosis. Labeled nucleotides are incorporated specifically into the X chromosomes during the last two hours of S phase, a property we exploit to identify a highly synchronous cohort of nuclei. By tracking X-labeled nuclei through early meiotic prophase, we define the sequence and duration of chromosome movement, nuclear reorganization, pairing at pairing centers (PCs), and SC assembly. Appearance of ZYG-12 foci (marking attachment of PCs to the nuclear envelope) and onset of active mobilization occur within an hour after S phase completion. Movement occurs for nearly 2 hours before stable pairing is observed at PCs, and autosome movement continues for roughly 4 hours thereafter. Chromosomes are tightly clustered during a 2-3 hour post-pairing window, during which the bulk of SC assembly occurs; however, initiation of SC assembly can precede evident chromosome clustering. SC assembly on autosomes begins immediately after PC pairing is detected and is completed within about 3.5 hours. For the X chromosomes, PC pairing is contemporaneous with autosomal pairing, but autosomes complete synapsis earlier (on average) than X chromosomes, implying that X chromosomes have a delay in onset and/or a slower rate of SC assembly. Additional evidence suggests that transient association among chromosomes sharing the same PC protein may contribute to partner discrimination.

scholarly journals The genome-wide, multi-layered architecture of chromosome pairing in early Drosophila embryos

2018 ◽  
Author(s):  
Jelena Erceg ◽  
Jumana AlHaj Abed ◽  
Anton Goloborodko ◽  
Bryan R. Lajoie ◽  
Geoffrey Fudenberg ◽  
...  
Keyword(s):  
Early Stage ◽  
Chromatin Accessibility ◽  
Homologous Chromosomes ◽  
Layered Architecture ◽  
Homolog Pairing ◽  
Genome Wide ◽  
New Strategy ◽  
Pioneer Factor ◽  
Standing Question ◽  
Drosophila Embryos

AbstractGenome organization involves cis and trans chromosomal interactions, both implicated in gene regulation, development, and disease. Here, we focused on trans interactions in Drosophila, where homologous chromosomes are paired in somatic cells from embryogenesis through adulthood. We first addressed the long-standing question of whether pairing extends genome-wide and, to this end, developed a haplotype-resolved Hi-C approach that uses a new strategy to minimize homolog misassignment and thus robustly distinguish trans-homolog from cis contacts. This approach revealed striking genome-wide pairing in Drosophila embryos. Moreover, we discovered pairing to be surprisingly structured, with trans-homolog domains and interaction peaks, many coinciding with the positions of analogous cis features. We also found a significant correlation between pairing and the chromatin accessibility mediated by the pioneer factor Zelda. Our findings reveal a complex, highly structured organization underlying homolog pairing, first discovered more than a century ago.One Sentence SummaryA robust approach for haplotype-resolved Hi-C reveals highly-structured homolog pairing in early stage Drosophila embryos.

scholarly journals The genome-wide multi-layered architecture of chromosome pairing in early Drosophila embryos

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Jelena Erceg ◽  
Jumana AlHaj Abed ◽  
Anton Goloborodko ◽  
Bryan R. Lajoie ◽  
Geoffrey Fudenberg ◽  
...  
Keyword(s):  
Computational Approach ◽  
Homologous Chromosomes ◽  
Layered Architecture ◽  
Homolog Pairing ◽  
Genome Wide ◽  
Mammalian Embryos ◽  
Pioneer Factor ◽  
Genome Activation ◽  
Drosophila Embryos ◽  
Zygotic Genome

Abstract Genome organization involves cis and trans chromosomal interactions, both implicated in gene regulation, development, and disease. Here, we focus on trans interactions in Drosophila, where homologous chromosomes are paired in somatic cells from embryogenesis through adulthood. We first address long-standing questions regarding the structure of embryonic homolog pairing and, to this end, develop a haplotype-resolved Hi-C approach to minimize homolog misassignment and thus robustly distinguish trans-homolog from cis contacts. This computational approach, which we call Ohm, reveals pairing to be surprisingly structured genome-wide, with trans-homolog domains, compartments, and interaction peaks, many coinciding with analogous cis features. We also find a significant genome-wide correlation between pairing, transcription during zygotic genome activation, and binding of the pioneer factor Zelda. Our findings reveal a complex, highly structured organization underlying homolog pairing, first discovered a century ago in Drosophila. Finally, we demonstrate the versatility of our haplotype-resolved approach by applying it to mammalian embryos.

scholarly journals Synaptonemal complex components are required for meiotic checkpoint function in C. elegans

2016 ◽  
Author(s):  
Tisha Bohr ◽  
Guinevere Ashley ◽  
Evan Eggleston ◽  
Kyra Firestone ◽  
Needhi Bhalla
Keyword(s):  
Synaptonemal Complex ◽  
Chromosome Segregation ◽  
Meiotic Chromosome ◽  
Checkpoint Response ◽  
Homologous Chromosomes ◽  
C Elegans ◽  
Homolog Pairing ◽  
The Stability ◽  
Complex Components

AbstractSynapsis involves the assembly of a proteinaceous structure, the synaptonemal complex (SC), between paired homologous chromosomes and is essential for proper meiotic chromosome segregation. In C. elegans, the synapsis checkpoint selectively removes nuclei with unsynapsed chromosomes by inducing apoptosis. This checkpoint depends on Pairing Centers (PCs), cis-acting sites that promote pairing and synapsis. We have hypothesized that the stability of homolog pairing at PCs is monitored by this checkpoint. Here, we report that SC components SYP-3, HTP-3, HIM-3 and HTP-1 are required for a functional synapsis checkpoint. Mutation of these components does not abolish PC function, demonstrating they are bonafide checkpoint components. Further, we identify mutant backgrounds in which the instability of homolog pairing at PCs does not correlate with the synapsis checkpoint response. Altogether, these data suggest that, in addition to homolog pairing, SC assembly may be monitored by the synapsis checkpoint.

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