Dynamic Repositioning Research Articles

Mechanisms controlling the multistage post-translational processing of endogenous Nrf1α/TCF11 proteins to yield distinct isoforms within the coupled positive and negative feedback circuits

To gain a better understanding of the multistep processing of Nrf1 to yield various isoforms with confused molecular masses, we herein establish a generally acceptable criterion required for identification of its endogenous full-length proteins and derivative isoforms expressed differentially in distinct experimental cell lines. Further work has been focused on the molecular mechanisms that dictate the successive post-translational modifications (i.e. glycosylation by OST, deglycosylation by NGLY, and ubiquitination by Hrd1) of this CNC-bZIP protein and its proteolytic processing to give rise to multiple proteoforms. Several lines of experimental evidence have demonstrated that the nascent Nrf1α/TCF11 polypeptide (non-glycosylated) is transiently translocated into the endoplasmic reticulum (ER), in which it becomes an inactive glycoprotein-A, and is folded in a proper topology within and around membranes. Thereafter, dynamic repositioning of the ER-resident domains in Nrf1 glycoprotein is driven by p97-fueled retrotranslocation into extra-ER compartments. Therein, Nrf1 glycoprotein is allowed for deglycosylation digestion by glycosidases into a deglycoprotein-B and its progressive proteolytic processing by cytosolic DDI-1/2 and proteasomes so as to generate N-terminally-truncated protein-C/D. This processing is accompanied by removal of a major N-terminal ~12.5-kDa polypeptide from Nrf1α. Interestingly, our present study has further unraveled that there exist coupled positive and negative feedback circuits between Nrf1 and cognate target genes, including those encoding its regulators p97, Hrd1, DDI-1 and proteasomes. These key players are differentially or even oppositely involved in diverse cellular signaling responses to distinct extents of ER-derived proteotoxic and oxidative stresses induced by different concentrations of proteasomal inhibitors.

Topovectorial mechanisms control the juxtamembrane proteolytic processing of Nrf1 to remove its N-terminal polypeptides during maturation of the CNC-bZIP factor

The topobiological behaviour of Nrf1 dictates its post-translational modification and its ability to transactivate target genes. Here, we have elucidated that topovectorial mechanisms control the juxtamembrane processing of Nrf1 on the cyto/nucleoplasmic side of endoplasmic reticulum (ER), whereupon it is cleaved and degraded to remove various lengths of its N-terminal domain (NTD, also refolded into a UBL module) and acidic domain-1 (AD1) to yield multiple isoforms. Notably, an N-terminal ~12.5-kDa polypeptide of Nrf1 arises from selective cleavage at an NHB2-adjoining region within NTD, whilst other longer UBL-containing isoforms may arise from proteolytic processing of the protein within AD1 around PEST1 and Neh2L degrons. The susceptibility of Nrf1 to proteolysis is determined by dynamic repositioning of potential UBL-adjacent degrons and cleavage sites from the ER lumen through p97-driven retrotranslocation and -independent pathways into the cyto/nucleoplasm. These repositioned degrons and cleavage sites within NTD and AD1 of Nrf1 are coming into their bona fide functionality, thereby enabling it to be selectively processed by cytosolic DDI-1/2 proteases and also partiality degraded via 26S proteasomes. The resultant proteolytic processing of Nrf1 gives rise to a mature ~85-kDa CNC-bZIP transcription factor, which regulates transcriptional expression of cognate target genes. Furthermore, putative ubiquitination of Nrf1 is not a prerequisite necessary for involvement of p97 in the client processing. Overall, the regulated juxtamembrane proteolysis (RJP) of Nrf1, though occurring in close proximity to the ER, is distinctive from the mechanism that regulates the intramembrane proteolytic (RIP) processing of ATF6 and SREBP1.

Comparing spatial diversification and meta-population models in the Indo-Australian Archipelago.

Reconstructing the processes that have shaped the emergence of biodiversity gradients is critical to understand the dynamics of diversification of life on Earth. Islands have traditionally been used as model systems to unravel the processes shaping biological diversity. MacArthur and Wilson's island biogeographic model predicts diversity to be based on dynamic interactions between colonization and extinction rates, while treating islands themselves as geologically static entities. The current spatial configuration of islands should influence meta-population dynamics, but long-term geological changes within archipelagos are also expected to have shaped island biodiversity, in part by driving diversification. Here, we compare two mechanistic models providing inferences on species richness at a biogeographic scale: a mechanistic spatial-temporal model of species diversification and a spatial meta-population model. While the meta-population model operates over a static landscape, the diversification model is driven by changes in the size and spatial configuration of islands through time. We compare the inferences of both models to floristic diversity patterns among land patches of the Indo-Australian Archipelago. Simulation results from the diversification model better matched observed diversity than a meta-population model constrained only by the contemporary landscape. The diversification model suggests that the dynamic re-positioning of islands promoting land disconnection and reconnection induced an accumulation of particularly high species diversity on Borneo, which is central within the island network. By contrast, the meta-population model predicts a higher diversity on the mainlands, which is less compatible with empirical data. Our analyses highlight that, by comparing models with contrasting assumptions, we can pinpoint the processes that are most compatible with extant biodiversity patterns.

Data-Driven Omniscient Bounds and Greedy Policies for Ambulance Allocation and Dynamic Redeployment

We present an efficient data-driven computational bounding and solution approach for static allocation of ambulance fleet and its dynamic redeployment, where the goal is to position (or re-position) ambulances to bases to maximize the systems service level. We leverage the framework presented, to find data-driven omniscient bounds on the performance of a static location or dynamic redeployment policy. Central to our approach, is a discrete-event simulator to evaluate the impact of ambulance deployments to given call logs of emergency requests. We model ambulance allocation as an approximate submodular maximization problem, and devise a simple and efficient greedy algorithm that produces good solutions for static allocation, and can also be repeatedly employed in real-time for dynamic repositioning. Although the objective is not submodular, we generate data-driven guarantees on solution quality by formulating an omniscient upper bound (in both static and dynamic cases) using integer programming. We show that omniscient dispatch, as well as omniscient location combined with dispatch, are submodular upper bounds. Our experiments based on real data from an Asian city’s EMS, demonstrate how optimality gaps can be computed, and that they are small in this setting. The bound formulation that we present is general and can be applied for any alternative data-driven simulation framework or solution. We also test settings with customer abandonment and demonstrate the working of our algorithmic and bounding approach in that setting.

Time-Resolved Fast Mammalian Behavior Reveals the Complexity of Protective Pain Responses

Potentially harmful stimuli are detected at the skin by nociceptor sensory neurons that drive rapid protective withdrawal reflexes and pain. We set out to define, at a millisecond timescale, the relationship between the activity of these sensory neurons and the resultant behavioral output. Brief optogenetic activation of cutaneous nociceptors was found to activate only a single action potential in each fiber. This minimal input was used to determine high-speed behavioral responses in freely behaving mice. The localized stimulus generated widespread dynamic repositioning and alerting sub-second behaviors whose nature and timing depended on the context of the animal and its position, activity, and alertness. Our findings show that the primary response to injurious stimuli is not limited, fixed, or localized, but is dynamic, and that it involves recruitment and gating of multiple circuits distributed throughout the central nervous system at a sub-second timescale to effectively both alert to the presence of danger and minimize risk of harm.

Incentivizing the Use of Bike Trailers for Dynamic Repositioning in Bike Sharing Systems

Bike Sharing System (BSS) is a green mode of transportation that is employed extensively for short distance travels in major cities of the world. Unfortunately, the users behaviour driven by their personal needs can often result in empty or full base stations, thereby resulting in loss of customer demand. To counter this loss in customer demand, BSS operators typically utilize a fleet of carrier vehicles for repositioning the bikes between stations. However, this fuel burning mode of repositioning incurs a significant amount of routing, labor cost and further increases carbon emissions. Therefore, we propose a potentially self-sustaining and environment friendly system of dynamic repositioning, that moves idle bikes during the day with the help of bike trailers. A bike trailer is an add-on to a bike that can help with carrying 3-5 bikes at once. Specifically, we make the following key contributions: (i) We provide an optimization formulation that generates “repositioning” tasks so as to minimize the expected lost demand over past demand scenarios; (ii) Within the budget constraints of the operator, we then design a mechanism to crowdsource the tasks among potential users who intend to execute repositioning tasks; (iii) Finally, we provide extensive results on a wide range of demand scenarios from a real-world data set to demonstrate that our approach is highly competitive to the existing fuel burning mode of repositioning while being green.

Floating-ECC: Dynamic Repositioning of Error Correcting Code Bits for Extending the Lifetime of STT-RAM Caches

Spin-Transfer Torque RAM (STT-RAM) is a promising alternative to SRAM for implementing on-chip L2 and L3 caches. One of the most critical challenges in STT-RAM is reliability due to limited write endurance, which results in insufficient lifetime, as well as various types of errors. Previous studies have focused on either presenting various cache architectures/management techniques to improve the lifetime of STT-RAM caches or utilizing different Error Correcting Codes (ECCs) to protect against the permanent and transient errors. However, there is no quantitative analysis in the literature to determine the impact of ECCs on the lifetime of the STT-RAM caches. This paper formulates this impact and demonstrates that ECCs shorten the lifetime of STT-RAM cache lines by more than 50 percent due to ECCs high write activity. Then, we propose the Floating-ECC architecture for increasing the lifetime of the STT-RAM caches. The main idea is to evenly distribute the ECC write activity over all bits of cache lines by periodically relocating the ECC bits inside the cache lines. The simulation results for the most conventional ECC scheme, i.e., interleaved Single Error Correction-Double Error Detection (SEC-DED), show that Floating-ECC increases the lifetime of L2 and L3 caches by more than 318 percent and 254 percent, respectively.

Anaphase asymmetry and dynamic repositioning of the division plane during maize meiosis.

The success of an organism is contingent upon its ability to transmit genetic material through meiotic cell division. In plant meiosis I, the process begins in a large spherical cell without physical cues to guide the process. Yet, two microtubule-based structures, the spindle and phragmoplast, divide the chromosomes and the cell with extraordinary accuracy. Using a live-cell system and fluorescently labeled spindles and chromosomes, we found that the process self- corrects as meiosis proceeds. Metaphase spindles frequently initiate division off-center, and in these cases anaphase progression is asymmetric with the two masses of chromosomes traveling unequal distances on the spindle. The asymmetry is compensatory, such that the chromosomes on the side of the spindle that is farthest from the cell cortex travel a longer distance at a faster rate. The phragmoplast forms at an equidistant point between the telophase nuclei rather than at the original spindle mid-zone. This asymmetry in chromosome movement implies a structural difference between the two halves of a bipolar spindle and could allow meiotic cells to dynamically adapt to errors in metaphase and accurately divide the cell volume.

Dynamic regulation of transcription factors by nucleosome remodeling.

The chromatin landscape and promoter architecture are dominated by the interplay of nucleosome and transcription factor (TF) binding to crucial DNA sequence elements. However, it remains unclear whether nucleosomes mobilized by chromatin remodelers can influence TFs that are already present on the DNA template. In this study, we investigated the interplay between nucleosome remodeling, by either yeast ISW1a or SWI/SNF, and a bound TF. We found that a TF serves as a major barrier to ISW1a remodeling, and acts as a boundary for nucleosome repositioning. In contrast, SWI/SNF was able to slide a nucleosome past a TF, with concurrent eviction of the TF from the DNA, and the TF did not significantly impact the nucleosome positioning. Our results provide direct evidence for a novel mechanism for both nucleosome positioning regulation by bound TFs and TF regulation via dynamic repositioning of nucleosomes.

Ideas, properties, and standards of fracture repositioning with osteopathy in traditional Mongolian medicine in China

ObjectiveTo explore the unique ideas, properties, and standards of fracture repositioning with osteopathy in traditional Mongolian medicine in China. MethodsBased on the natural life concept of “integration of universe and man,” osteopathy in traditional Mongolian medicine in China uses the modern principles and methods of physiology, psychology, and biomechanics. Against this background, we explored the unique ideas, properties, and standards of fracture repositioning in traditional Mongolian medicine. ResultsFracture treatment with osteopathy in traditional Mongolian medicine in China is based on (a) the ideas of natural, sealed, self and dynamic repositioning of fractures; (b) the properties of structural continuity and functional completeness; (c) the standards of “integration of movement and stillness” and “force to force.” ConclusionThe unique ideas, properties, and standards of fracture repositioning with osteopathy in traditional Mongolian medicine in China have resulted in the widespread use of such techniques and represents the future direction of the development of fracture repositioning.

Dynamic Regulation of Transcription Factors by Nucleosome Remodeling

In eukaryotic cells, transcription activation and repression are regulated by transcription factors (TFs) and nucleosomes. Although it has been demonstrated that a TF and a nucleosome can directly compete for binding to the same region of DNA, it is unclear whether and how such a competition may continue after a TF has been bound and a nucleosome has been assembled. In this study, we have addressed an aspect of this question by investigating whether a nucleosome under remodeling can displace a bound TF. We determined the locations of both a nucleosome and a TF on DNA by mechanically unzipping the DNA molecule. We found that under the action of ISWI remodeling, a nucleosome was not repositioned past a TF. In contrast, under the action of SWI/SNF remodeling, a nucleosome was repositioned past a TF with concurrent eviction of the TF from the DNA. Our results demonstrate a novel mechanism for how TFs may be regulated via dynamic repositioning of nucleosomes.

The meiotic nuclear lamina regulates chromosome dynamics and promotes efficient homologous recombination in the mouse.

The nuclear lamina is the structural scaffold of the nuclear envelope and is well known for its central role in nuclear organization and maintaining nuclear stability and shape. In the past, a number of severe human disorders have been identified to be associated with mutations in lamins. Extensive research on this topic has provided novel important clues about nuclear lamina function. These studies have contributed to the knowledge that the lamina constitutes a complex multifunctional platform combining both structural and regulatory functions. Here, we report that, in addition to the previously demonstrated significance for somatic cell differentiation and maintenance, the nuclear lamina is also an essential determinant for germ cell development. Both male and female mice lacking the short meiosis-specific A-type lamin C2 have a severely defective meiosis, which at least in the male results in infertility. Detailed analysis revealed that lamin C2 is required for telomere-driven dynamic repositioning of meiotic chromosomes. Loss of lamin C2 affects precise synapsis of the homologs and interferes with meiotic double-strand break repair. Taken together, our data explain how the nuclear lamina contributes to meiotic chromosome behaviour and accurate genome haploidization on a mechanistic level.

Real‐time 3D target tracking in MRI guided focused ultrasound ablations in moving tissues

Magnetic resonance imaging-guided high intensity focused ultrasound is a promising method for the noninvasive ablation of pathological tissue in abdominal organs such as liver and kidney. Due to the high perfusion rates of these organs, sustained sonications are required to achieve a sufficiently high temperature elevation to induce necrosis. However, the constant displacement of the target due to the respiratory cycle render continuous ablations challenging, since dynamic repositioning of the focal point is required. This study demonstrates subsecond 3D high intensity focused ultrasound-beam steering under magnetic resonance-guidance for the real-time compensation of respiratory motion. The target is observed in 3D space by coupling rapid 2D magnetic resonance-imaging with prospective slice tracking based on pencil-beam navigator echoes. The magnetic resonance-data is processed in real-time by a computationally efficient reconstruction pipeline, which provides the position, the temperature and the thermal dose on-the-fly, and which feeds corrections into the high intensity focused ultrasound-ablator. The effect of the residual update latency is reduced by using a 3D Kalman-predictor for trajectory anticipation. The suggested method is characterized with phantom experiments and verified in vivo on porcine kidney. The results show that for update frequencies of more than 10 Hz and latencies of less then 114 msec, temperature elevations can be achieved, which are comparable to static experiments.

Dynamic Repositioning of Dorsal to Two Different κB Motifs Controls Its Autoregulation during Immune Response in Drosophila

Autoregulation is one of the mechanisms of imparting feedback control on gene expression. Positive autoregulatory feedback results in induction of a gene, and negative feedback leads to its suppression. Here, we report an interesting mechanism of autoregulation operating on Drosophila Rel gene dorsal that can activate as well as repress its expression. Using biochemical and genetic approaches, we show that upon immune challenge Dorsal regulates its activation as well as repression by dynamically binding to two different kappaB motifs, kappaB(I) (intronic kappaB) and kappaB(P) (promoter kappaB), present in the dorsal gene. Although the kappaB(I) motif functions as an enhancer, the kappaB(P) motif acts as a transcriptional repressor. Interestingly, Dorsal binding to these two motifs is dynamic; immediately upon immune challenge, Dorsal binds to the kappaB(I) leading to auto-activation, whereas at the terminal phase of the immune response, it is removed from the kappaB(I) and repositioned at the kappaB(P), resulting in its repression. Furthermore, we show that repression of Dorsal as well as its binding to the kappaB(P) depends on the transcription factor AP1. Depletion of AP1 by RNA interference resulted in constitutive expression of Dorsal. In conclusion, this study suggests that during acute phase response dorsal is regulated by following two subcircuits: (i) Dl-kappaB(I) for activation and (ii) Dl-AP1-kappaB(P) for repression. These two subcircuits are temporally delineated and bring about overall regulation of dorsal during immune response. These results suggest the presence of a previously unknown mechanism of Dorsal autoregulation in immune-challenged Drosophila.

Dynamic properties of meiosis-specific lamin C2 and its impact on nuclear envelope integrity

A hallmark of meiosis is the precise pairing and the stable physical connection (synapsis) of the homologous chromosomes. These processes are essential prerequisite for their proper segregation. Pairing of the homologs during meiotic prophase I critically depends on characteristic movements of chromosomes. These movements, in turn, require attachment of meiotic telomeres to the nuclear envelope and their subsequent dynamic repositioning. Dynamic repositioning of meiotic telomeres goes along with profound structural reorganization of the nuclear envelope. The short A-type lamin C2 is thought to play a critical role in this process due to its specific expression during meiotic prophase I and the unique localization surrounding telomere attachments. Consistent with this notion, here we provide compelling evidence that meiosis-specific lamin C2 features a significantly increased mobility compared to somatic lamins as revealed by photobleaching techniques. We show that this property can be clearly ascribed to the lack of the N-terminal head and the significantly shorter α-helical coil domain. Moreover, expression of lamin C2 in somatic cells induces nuclear deformations and alters the distribution of the endogenous nuclear envelope proteins lamin B1, LAP2, SUN1 and SUN2. Together, our data define lamin C2 as a “natural lamin deletion mutant” that confers unique properties to the nuclear envelope which would be essential for dynamic telomere repositioning during meiotic prophase I.

Dynamic properties of meiosis-specific lamin C2 and its impact on nuclear envelope integrity

A hallmark of meiosis is the precise pairing and the stable physical connection (synapsis) of the homologous chromosomes. These processes are essential prerequisite for their proper segregation. Pairing of the homologs during meiotic prophase I critically depends on characteristic movements of chromosomes. These movements, in turn, require attachment of meiotic telomeres to the nuclear envelope and their subsequent dynamic repositioning. Dynamic repositioning of meiotic telomeres goes along with profound structural reorganization of the nuclear envelope. The short A-type lamin C2 is thought to play a critical role in this process due to its specific expression during meiotic prophase I and the unique localization surrounding telomere attachments. Consistent with this notion, here we provide compelling evidence that meiosis-specific lamin C2 features a significantly increased mobility compared to somatic lamins as revealed by photobleaching techniques. We show that this property can be clearly ascribed to the lack of the N-terminal head and the significantly shorter α-helical coil domain. Moreover, expression of lamin C2 in somatic cells induces nuclear deformations and alters the distribution of the endogenous nuclear envelope proteins lamin B1, LAP2, SUN1 and SUN2. Together, our data define lamin C2 as a "natural lamin deletion mutant" that confers unique properties to the nuclear envelope which would be essential for dynamic telomere repositioning during meiotic prophase I.

Dynamic and Selective Nucleosome Repositioning during Endotoxin Tolerance

Sepsis is encoded by a sequel of transcription activation and repression events that initiate, sustain, and resolve severe systemic inflammation. The repression/silencing phase occurs in blood leukocytes of animals and humans following the initiation of systemic inflammation due to developing endotoxin tolerance. We previously reported that NF-kappaB transcription factor RelB and histone H3 lysine methyltransferase G9a directly interact to induce facultative heterochromatin assembly and regulate epigenetic silencing during endotoxin tolerance, which is a major feature of sepsis. The general objective of this study was to assess whether dynamic temporal, structural, and positional changes of nucleosomes influence the sepsis phenotype. We used the THP-1 sepsis cell model to isolate mononucleosomes by rapid cell permeabilization and digestion of chromatin with micrococcal nuclease and then compared tumor necrosis factor alpha (TNFalpha) proximal promoter nucleosome alignment in endotoxin-responsive and -tolerant phenotypes. We found differential and dynamic repositioning of nucleosomes from permissive to repressive locations during the activation and silencing phases of transcription reprogramming and identified the following mechanisms that may participate in the process. 1) Two proximal nucleosomes repositioned to expose the primary NF-kappaB DNA binding site in endotoxin-responsive cells, and this "promoter opening" required the ATP-independent chaperone NAP1 to replace the core histone H2A with the H2A.Z variant. 2) During RelB-dependent endotoxin tolerance, the two nucleosomes repositioned and masked the primary NF-kappaB DNA binding site. 3) Small interfering RNA-mediated inhibition of RelB expression prevented repressive nucleosome repositioning and tolerance induction, but the "open" promoter required endotoxin-induced NF-kappaB p65 promoter binding to initiate transcription, supporting the known requirement of p65 posttranslational modifications for transactivation. 4) Sustaining the permissive promoter state after RelB knockdown required ATP-dependent nucleosome remodeler BAF complex. Moreover, we found that forced expression of RelB in responsive cells induced repressive nucleosome positioning and silenced TNFalpha transcription, demonstrating the plasticity of nucleosome remodeling and its dependence on RelB. Our data suggest that nucleosome repositioning controls both the induction and epigenetic silencing phases of TNFalpha transcription associated with sepsis.

Dynamic gene expression is required for anterior regionalization in a spider

Patterning of a multicellular embryo requires precise spatiotemporal control of gene expression during development. The gradient of the morphogen bicoid regulates anterior regionalization in the syncytial blastoderm of Drosophila. However many arthropod embryos develop from a cellular blastoderm that does not allow the formation of transcription factor gradients. Here we show that correct anterior development of the cellularized embryo of the spider Achaearanea tepidariorum requires an anterior-to-posterior wave of dynamic gene expression for positioning the stripes of hairy, hedgehog, and orthodenticle expression. Surprisingly, this dynamic repositioning of the expression of these segmentation genes is blocked in orthodenticle(pRNAi) embryos and no anterior structures are specified in those embryos. Our data suggest that dynamic gene expression across a field of cells is required for anterior regionalization in spiders and provides an explanation for the problem of how positional values for anterior segmentation genes are specified via a morphogen-independent mechanism across a field of cells.

Performance of a novel piezoelectric motor at 4.7 T: applications and initial tests

The focus of this report was to test the performance of a novel piezoelectric motor under high magnetic field strength conditions and to investigate its potential applications in small animal magnetic resonance imaging (MRI). The device is made entirely of nonferrous materials and consists of four piezoelectric ceramic plates connected to a threaded metal tube through which a screw migrates. Ultrasonic vibrations of the threads inherent to the tube result in rotational and translational motion of the screw. Potential applications of the piezoelectric motor were investigated at 4.7 T. Firstly, phantom studies showed the motor was capable of accurately delivering low injection volumes ( approximately 0.01 ml). Dynamic contrast-enhanced MRI (DCE-MRI) studies performed in vivo using serially acquired T1-weighted, spin-echo imaging demonstrated the ability of the motor to reliably administer MR contrast-enhancing agent into live tumor-bearing mice without the introduction of image artifacts. In a second set of experiments, the motor allowed for controlled, dynamic repositioning of an anatomic slice of interest in a live animal to magnetic field isocenter, which resulted in reduced geometric distortion and image artifact due to improved radiofrequency and gradient field homogeneity. In conclusion, piezoelectric motors are MR compatible and offer great potential for improving MRI efficiency and throughput, particularly in a preclinical setting. Further investigation into applications such as automated capacitor tuning and impedance matching for MR transceiver coils is warranted.

Transmembrane protein Sun2 is involved in tethering mammalian meiotic telomeres to the nuclear envelope

Dynamic repositioning of telomeres is a unique feature of meiotic prophase I that is highly conserved among eukaryotes. At least in fission yeast it was shown to be required for proper alignment and recombination of homologous chromosomes. On entry into meiosis telomeres attach to the nuclear envelope and transiently cluster at a limited area to form a chromosomal bouquet. Telomere clustering is thought to promote chromosome recognition and stable pairing of the homologs. However, the molecular basis of telomere attachment and movement is largely unknown. Here we report that mammalian SUN-domain protein Sun2 specifically localizes to the nuclear envelope attachment sites of meiotic telomeres. Sun2-telomere association is maintained throughout the dynamic movement of telomeres. This association does not require the assembly of chromosomal axial elements or the presence of A-type lamins. Detailed EM analysis revealed that Sun2 is part of a membrane-spanning fibrillar complex that interconnects attached telomeres with cytoplasmic structures. Together with recent findings in fission yeast, our study indicates that the molecular mechanisms required for tethering meiotic telomeres and their dynamic movements during bouquet formation are conserved among eukaryotes.