The Effects of Landscape Variables on the Species-Area Relationship during Late-Stage Habitat Fragmentation

Few studies have focused explicitly on the later stages of the fragmentation process, or "late-stage fragmentation", during which habitat area and patch number decrease simultaneously. This lack of attention is despite the fact that many of the anthropogenically fragmented habitats around the world are, or soon will be, in late-stage fragmentation. Understanding the ecological processes and patterns that occur in late-stage fragmentation is critical to protect the species richness in these fragments. We investigated plant species composition on 152 islands in the Thousand Island Lake, China. A random sampling method was used to create simulated fragmented landscapes with different total habitat areas and numbers of patches mimicking the process of late-stage fragmentation. The response of the landscape-scale species-area relationship (LSAR) to fragmentation per se was investigated, and the contribution of inter-specific differences in the responses to late-stage fragmentation was tested. We found that the loss of species at small areas was compensated for by the effects of fragmentation per se, i.e., there were weak area effects on species richness in landscapes due to many patches with irregular shapes and high variation in size. The study also illustrated the importance of inter-specific differences for responses to fragmentation in that the LSARs of rare and common species were differently influenced by the effects of fragmentation per se. In conclusion, our analyses at the landscape scale demonstrate the significant influences of fragmentation per se on area effects and the importance of inter-specific differences for responses to fragmentation in late-stage fragmentation. These findings add to our understanding of the effects of habitat fragmentation on species diversity.     

The geometry of habitat fragmentation: Effects of species distribution patterns on extinction risk due to habitat conversion

Land‐use changes, which cause loss, degradation, and fragmentation of natural habitats, are important anthropogenic drivers of biodiversity change. However, there is an ongoing debate about how fragmentation per se affects biodiversity in a given amount of habitat. Here, we illustrate why it is important to distinguish two different aspects of fragmentation to resolve this debate: (a) geometric fragmentation effects, which exclusively arise from the spatial distributions of species and habitat fragments, and (b) demographic fragmentation effects due to reduced fragment sizes, and/or changes in fragment isolation, edge effects, or species interactions. While most empirical studies are primarily interested in quantifying demographic fragmentation effects, geometric effects are typically invoked as post hoc explanations of biodiversity responses to fragmentation per se. Here, we present an approach to quantify geometric fragmentation effects on species survival and extinction probabilities. We illustrate this approach using spatial simulations where we systematically varied the initial abundances and distribution patterns (i.e., random, aggregated, or regular) of species as well as habitat amount and fragmentation per se. As expected, we found no geometric fragmentation effects when species were randomly distributed. However, when species were aggregated, we found positive effects of fragmentation per se on survival probability for a large range of scenarios. For regular species distributions, we found weakly negative geometric effects. These findings are independent of the ecological mechanisms which generate nonrandom species distributions. Our study helps to reconcile seemingly contradictory results of previous fragmentation studies. Since intraspecific aggregation is a ubiquitous pattern in nature, our findings imply widespread positive geometric fragmentation effects. This expectation is supported by many studies that find positive effects of fragmentation per se on species occurrences and diversity after controlling for habitat amount. We outline how to disentangle geometric and demographic fragmentation effects, which is critical for predicting the response of biodiversity to landscape change.     

Fragmentation of cellulose by the major Thermomonospora fusca cellulases, Trichoderma reesei CBHI, and their mixtures

In this study, the fragmentation activities of Thermomonospora fusca cellulases E(2), E(3), E(5), Trichoderma reesei CBHI, and their mixtures were measured to study synergism in fragmentation. Fragmentation studies revealed that only two pure cellulases, T. fusca E(2) and E(5) had significant fragmentation activity. T. fusca E(3) shows strong synergism in fragmentation both in the production of reducing sugars and in fragmentation with both T. fusca endoglucananses and with T. reesei CBHI. Most mixtures containing CBHI produced higher rates of fragmentation than comparable mixtures containing E(3). The highest rate and extent of reducing sugar formation and the highest fragmentation activity were obtained with a mixture of E(2), E(3), and CBHI. (c) 1992 John Wiley & Sons, Inc.     

Epstein-Barr virus induces fragmentation of chromosomal DNA during lytic infection.

Pulsed-field agarose gel electrophoresis showed that fragmentation of chromosomal DNA in Raji cells was induced by infection with the P3HR-1 strain of Epstein-Barr virus (EBV). S1 nuclease treatment of the agarose plugs containing cells suggested that the majority of DNA fragments did not contain single-strand gaps. Chromosomal DNA fragmentation was inhibited by cycloheximide, indicating that protein synthesis was required for DNA fragmentation. Phosphonoacetic acid, an inhibitor of EBV DNA polymerase, did not inhibit fragmentation of chromosomal DNA. These findings suggest that EBV-specific early proteins participate in fragmentation of chromosomal DNA. Chromosomal DNA of P3HR-1 cells was also fragmented by treatment with n-butyrate plus 12-O-tetradecanoylphorbol-13-acetate (TPA), which induced activation of latent EBV genome following viral replication. In addition, fragmentation of DNA preceded cell death during lytic infection. These results suggest that fragmentation of chromosomal DNA is generally induced during EBV replication and probably contributes to the cytopathic effect of EBV. The role of DNA fragmentation in death of infected cells is discussed in relation to apoptosis.     

Detecting Fragmentation Extinction Thresholds for Forest Understory Plant Species in Peninsular Spain

Ecological theory predicts that fragmentation aggravates the effects of habitat loss, yet empirical results show mixed evidences, which fail to support the theory instead reinforcing the primary importance of habitat loss. Fragmentation hypotheses have received much attention due to their potential implications for biodiversity conservation, however, animal studies have traditionally been their main focus. Here we assess variation in species sensitivity to forest amount and fragmentation and evaluate if fragmentation is related to extinction thresholds in forest understory herbs and ferns. Our expectation was that forest herbs would be more sensitive to fragmentation than ferns due to their lower dispersal capabilities. Using forest cover percentage and the proportion of this percentage occurring in the largest patch within UTM cells of 10-km resolution covering Peninsular Spain, we partitioned the effects of forest amount versus fragmentation and applied logistic regression to model occurrences of 16 species. For nine models showing robustness according to a set of quality criteria we subsequently defined two empirical fragmentation scenarios, minimum and maximum, and quantified species’ sensitivity to forest contraction with no fragmentation, and to fragmentation under constant forest cover. We finally assessed how the extinction threshold of each species (the habitat amount below which it cannot persist) varies under no and maximum fragmentation. Consistent with their preference for forest habitats probability occurrences of all species decreased as forest cover contracted. On average, herbs did not show significant sensitivity to fragmentation whereas ferns were favored. In line with theory, fragmentation yielded higher extinction thresholds for two species. For the remaining species, fragmentation had either positive or non-significant effects. We interpret these differences as reflecting species-specific traits and conclude that although forest amount is of primary importance for the persistence of understory plants, to neglect the impact of fragmentation for some species can lead them to local extinction.     

Membrane fragmentation by an amyloidogenic fragment of human Islet Amyloid Polypeptide detected by solid-state NMR spectroscopy of membrane nanotubes

A key factor in the development of Type II diabetes is the loss of insulin producing pancreatic beta-cells. The amyloidogenic human Islet Amyloid Polypeptide (hIAPP also known as human amylin) is believed to play a crucial role in this biological process. Previous studies have shown that hIAPP forms small aggregates that kill beta-cells by disrupting the cellular membrane. In this study, we report membrane fragmentation by hIAPP using solid-state NMR experiments on nanotube arrays of anodic aluminum oxide containing aligned phospholipid membranes. In a narrow concentration range of hIAPP, an isotropic (31)P chemical shift signal indicative of the peptide-induced membrane fragmentation was detected. Solid-state NMR results suggest that membrane fragmentation is related to peptide aggregation as the presence of Congo Red, an inhibitor of amyloid formation, prevented membrane fragmentation and the non-amyloidogenic rat-IAPP did not cause membrane fragmentation. The disappearance of membrane fragmentation at higher concentrations of hIAPP suggests an alternate kinetic pathway to fibril formation in which membrane fragmentation is inhibited.     

Habitat fragmentation: A long and tangled tale

In this essay: I provide a brief history of habitat fragmentation research; I describe why its “non‐questions” (‘Is habitat fragmentation a big problem for wildlife species?” and, “Are the effects of habitat fragmentation generally negative or positive?”) are important to conservation; I outline my role in tackling these questions; I discuss reasons why the culture of habitat fragmentation research is largely incapable of accepting the answers; and I speculate on the future of habitat fragmentation research.     

宁夏黄河流域景观破碎化时空变化特征

基于RS和GIS技术,以土地利用数据为基础,采用有效粒度尺寸对宁夏黄河流域1985年和2010年的景观破碎化进行时空变化分析。结果显示:流域整体的有效粒度尺寸(meff)从1985年的6326.62 km2下降到2010年的2974.32 km2,破碎化程度呈显著加剧变化;从流域内部来看,景观破碎化程度最大的是黄左区间,破碎化程度最小的是苦水河和红柳沟;除引黄区间外,其余分区景观破碎化程度在25年间均有所加剧。特征尺度分析结果显示研究区景观破碎化空间变异分析的合适尺度为4500 m;景观破碎化指数的空间变异结果表明破碎化程度较大的区域面积明显多于破碎化程度弱的区域,景观破碎化空间异质性在25年间表现出明显的上升趋势。在海拔背景条件下,2400 m以下区域的景观破碎化程度较高,2400m以上区域破碎化程度较低,且随海拔的升高有降低的趋势;流域景观破碎化受人为干扰影响强烈,在人为干扰较强的1000—1500 m区段的景观破碎化程度最大;景观破碎化在时间上的变化受人为干扰影响产生的变化最为显著,由自然条件改变产生的影响有限。研究结果可为西北地区景观格局及景观破碎化的研究提供参考,并为区域景观格局优化和土地的有效管理提供依据。     

Rethinking the conceptual foundations of habitat fragmentation research

The conceptual foundations of habitat fragmentation research have not kept pace with empirical advances in our understanding of species responses to landscape change, nor with theoretical advances in the wider disciplines of ecology. There is now real debate whether explicit recognition of ‘habitat fragmentation’ as an over‐arching conceptual domain will stimulate or hinder further progress toward understanding and mitigating the effects of landscape change. In this paper, we critically challenge the conceptual foundations of the discipline, and attempt to derive an integrated perspective on the best way to advance mechanistic understanding of fragmentation processes. We depict the inherent assumptions underlying the discipline as a ‘conceptual phase space’ of contrasting false dichotomies in fragmentation ‘problem space’. In our opinion, the key determinant of whether ‘habitat fragmentation’ can remain a cohesive framework lies in the concept of ‘interdependence’: 1) interdependence of landscape effects on species and 2) interdependence of species responses to landscape change. If there is non‐trivial interdependence among the various sub‐components of habitat fragmentation, or non‐trivial interdependence among species responses to landscape change, then there will be real heuristic value in ‘habitat fragmentation’ as a single conceptual domain. At present, the current paradigms entrenched in the fragmentation literature are implicitly founded on strict independence of landscape effects (e.g. the debate about the independent effects of habitat loss versus fragmentation per se) and strict independence of species responses (e.g. the individualistic species response models underpinning landscape continuum models), despite compelling evidence for interdependence in both effects and responses to fragmentation. We discuss how strong ‘interdependence’ of effects and responses challenges us to rethink long‐held views, and re‐cast the conceptual foundations of habitat fragmentation in terms of spatial context‐dependence in the effects of multiple interacting spatial components of fragmentation, and community context‐dependence in the responses of multiple interacting species to landscape change.     

Trends in forest fragment research in Madagascar: Documented responses by lemurs and other taxa

The rise in research investigating fragmentation and its impact on primates and other taxa reflects the growing presence of fragmented landscapes themselves. Although numerous studies report the negative effects of fragmentation on biodiversity, it is difficult to generalize responses to fragmentation for specific taxonomic groups, such as non-human primates, when studies have not employed a definitive concept of fragmentation or fragments themselves. Madagascar's high degree of fragmentation, wealth of endemic taxa, and extensive history of ecological research provide the opportunity to compare fragmentation studies across similar contexts. We conducted a literature search of peer-reviewed articles on fragmentation in Madagascar to characterize its trends. A total of 70 articles, 46 of which concentrated on lemurs, tested the impacts of fragmentation on Malagasy taxa, while additional sources conducted research in one or more fragments without testing its effects (n = 112 total, 79 on lemurs). Studies on lemurs most frequently tested fragmentation's impacts on genetics and biodiversity metrics (n = 16 and 15 studies, respectively), although health, modeling, behavioral, and cross-disciplinary techniques were also reported. Responses to fragmentation were reported for 49 lemur species, with most studies concentrated in eastern Madagascar (87%). Although there was variation in the metrics reported in studies testing the effects of fragmentation on Malagasy species, the most common measures were fragment area, isolation, or comparison to a control site. Landscape-scale approaches and examination of fragmentation per se were rarely employed. Characterizing trends of fragmentation research in Madagascar emphasizes the challenges of documenting fragmentation's effects while highlighting the benefits of research within fragmented landscapes, particularly when combined with consideration for how the matrix within human-modified landscapes may impact primate populations.     

黑河中游湿地景观破碎化过程及其驱动力分析

在遥感和GIS技术支持下,基于1975-2010年长时间序列遥感影像,选取斑块密度指数(PD)、景观内部生境面积指数(IA)、斑块平均面积指数(MPS)、斑块形状破碎化指数(FS1、FS2)等具有典型生态意义的景观指数模型,系统分析了黑河中游湿地景观的破碎化过程,并结合灰色关联分析、主成分分析等方法,探讨了影响研究区湿地景观破碎化过程的各驱动因子.结果表明:近35年来,研究区湿地景观破碎化主要表现为斑块平均面积的萎缩,斑块密度的上升以及斑块形状破碎化指数的增大.整个研究时段内,研究区湿地斑块平均面积减少了48.95hm2,斑块密度的上升0.006个/hm2;导致黑河中游湿地景观破碎化发生和发展的驱动力包含自然和人文两个方面.自然因子对湿地景观破碎化进程的影响则主要体现在气温和降水上,而且气温对湿地景观破碎化进程的影响程度明显大于降水.但在1975-2010年间的这一较小时间尺度上,人类活动对湿地景观破碎化的贡献率明显高于自然因子,人类活动能力的增强以及影响范围的不断扩大是引发黑河中游湿地景观破碎化的主因.     

YAC fragmentation with repetitive and single-copy sequences: detailed physical mapping of the presenilin 1 gene on chromosome 14

We constructed new LYS2 fragmentation vectors that allow direct acentric and centric fragmentation of yeast artificial chromosomes (YACs) and selection of fragmented YACs in yeast strain AB1380. The fragmentation vectors were used efficiently with repetitive (e.g., Alu), low-copy (e.g., CA-repeats) and single-copy (e.g., exons) sequences. High recombination efficiencies were obtained in fragmenting two different CEPH YACs with the Alu consensus sequence as target sequences for homologous recombination. Analysis of the acentric Alu fragmentation panel of 788H12, containing the presenilin 1 (PSEN1) gene for familial Alzheimer's disease (AD), indicated that high-resolution YAC fragmentation panels covering the entire parent YAC are obtained. Also, marker content analysis of the fragmentation panel indicated that fragmented YACs were propagated stably without rearrangements. The same fragmentation vectors were used efficiently for fragmentation of 788H12 with unique sequences, i.e., exons 3 and 12 of PSEN1 and D14S77, a polymorphic CA repeat, as target sequences. Together, our YAC fragmentation data of 788H12 provided a size estimate for the coding region of PSEN1 of 60kb and a more precise localization of D14S77 at 25kb upstream of PSEN1.     

Oligonucleosome DNA fragmentation of caspase 3 deficient MCF-7 cells in palmitate-induced apoptosis

Oligonucleosomal fragmentation of nuclear DNA is the late stage hallmark of the apoptotic process. In mammalian apoptotic cells fragmentation is catalyzed by DFF40/ CAD DNase. DFF40/CAD primary activated through site-specific proteolytic cleavage by caspase 3. The absence of caspase 3 in MCF-7 leads to lack of oligonucleosomal DNA fragmentation under numerous apoptotic stimuli. In this study it was shown that palmitate induces apoptotic changes of nuclei and oligonucleosomal DNA fragmentation in casp3 deficient MCF-7. Activation and accumulation of 40-50 kDa DFF40 like DNases in nuclei and cytoplasm of palmitate-treated MCF-7 were detected by SDS-DNA-PAGE assay. Microsomes of apoptotic MCF-7 activate 40-50 kDa nucleases when incubated with human placental chromatin and induce oligonucleosomal fragmentation of chromatin in cell free system. Both DNases activation and chromatin fragmentation are suppressed in presence of caspase 3/7 inhibitor Ac-DEVD-CHO. Microsome associated caspase 7 is suggested to play the principal role in induction of oligonucleosomal DNA fragmentation of casp3 defitient MCF-7.     

栖息地破碎化与鸟类生存

栖息地破碎化给野生动物带来的不良后果是全球生态学家和保护生物学家共同关心的问题.自从提出栖息地破碎化是导致生物多样性丧失的关键因素之一的论点后,近20年来,栖息地破碎化研究一直是生态学和保护生物学最活跃的前沿研究领域之一.栖息地破碎化是一动态过程,可在多尺度上发生并蕴涵着复杂的空间模式变化.栖息地破碎化对鸟类的生态学效应主要体现在面积效应、隔离效应和边缘效应等.这些效应影响着鸟类的分布、基因交流、种群动态、扩散行为、种间关系和生活史特征等,最终影响着鸟类的生存.介绍和总结了栖息地破碎化过程、研究的理论依据及栖息地破碎化对鸟类生存产生的诸多影响.     

人工林与天然林破碎化过程差异对比——以美国华盛顿州和密西西比州为例

森林损失和破碎化一直是国际社会普遍关注的重大环境问题之一。根据Forman景观变化包括穿孔、分割、破碎化、收缩和消失5种空间过程的理论,利用ArcGIS Modeler建立森林破碎化过程模型用以明确描述森林景观破碎化的空间过程和生态进程。基于NLCD2001、2006、2011 3期数据,以美国华盛顿州和密西西比州为研究区,利用森林破碎化过程模型,将森林损失斑块分为4种破碎化过程(分割类型因其线状特征被归入破碎化类型),对比分析天然林和人工林的破碎化过程在时空上的差异性。研究表明天然林破碎化斑块多分布于城市/森林、耕地/森林、以及灌木/森林的交界处,而人工林破碎化斑块分布格局较为零散;天然林中破碎化斑块和收缩斑块大多发生在上阶段收缩、破碎化以及穿孔斑块的边缘,而人工林中4种空间过程的承接关系不像天然林那么明显,但两者整体上都呈现相似的"收缩-消失-穿孔/破碎化"变化规律,主要表现为收缩类型占主导然后慢慢消退,穿孔和破碎化逐渐增多占据新的主导。     

Apoptosis in barley aleurone during germination and its inhibition by abscisic acid

During germination of barley grains, DNA fragmentation was observed in the aleurone. The appearance of DNA fragmentation in the aleurone layer, observed by TUNEL staining in aleurone sections, started near the embryo and extended to the aleurone cells far from the embryo in a time dependent manner. The same spatial temporal activities of hydrolytic enzymes such as -amylase were observed in aleurone. DNA fragmentation could also be seen in vitro under osmotic stress, in isolated aleurone. During aleurone protoplast isolation, a very enhanced and strong DNA fragmentation occurred which was not seen in protoplast preparations of tobacco leaves. ABA was found to inhibit DNA fragmentation occurring in barley aleurone under osmotic stress condition and during protoplast isolation, while the plant growth regulator gibberellic acid counteracted the effect of ABA. Addition of auxin or cytokinin had no significant effect on DNA fragmentation in these cells. To study the role of phosphorylation in ABA signal transduction leading to control of DNA fragmentation (apoptosis), the effects of the phosphatase inhibitor okadaic acid and of phenylarisine oxide on apoptosis were studied. We hypothesize that the regulation of DNA fragmentation in aleurone plays a very important role in spatial and temporal control of aleurone activities during germination. The possible signal transduction pathway of ABA leading to the regulation of DNA fragmentation is discussed.     

景观破碎化对植物种群的影响

景观破碎化是目前存在的一种普遍现象,是由于人为因素或其它非人为因素的干扰所导致的景观破碎分离并由简单趋向复杂的过程。它直接或间接影响着景观的结构、功能及其动态。本文首先简要介绍景观破碎化的成因和不同研究角度与水平上景观破碎化影响的表现;然后着重分析景观破碎化对植物种群的大小和灭绝速率、扩散和迁入、遗传和变异以及存活力等的影响;同时归纳现阶段研究景观破碎化对植物种群影响的主要方法和模型;最后提出目前景观破碎化对植物种群影响研究中存在的三个主要问题：缺乏原始的资料、成熟的模型和破碎化与其他因素,如污染、气候变化等,交互作用的识别。     

How fire interacts with habitat loss and fragmentation

Biodiversity faces many threats and these can interact to produce outcomes that may not be predicted by considering their effects in isolation. Habitat loss and fragmentation (hereafter ‘fragmentation’) and altered fire regimes are important threats to biodiversity, but their interactions have not been systematically evaluated across the globe. In this comprehensive synthesis, including 162 papers which provided 274 cases, we offer a framework for understanding how fire interacts with fragmentation. Fire and fragmentation interact in three main ways: (i) fire influences fragmentation (59% of 274 cases), where fire either destroys and fragments habitat or creates and connects habitat; (ii) fragmentation influences fire (25% of cases) where, after habitat is reduced in area and fragmented, fire in the landscape is subsequently altered because people suppress or ignite fires, or there is increased edge flammability or increased obstruction to fire spread; and (iii) where the two do not influence each other, but fire interacts with fragmentation to affect responses like species richness, abundance and extinction risk (16% of cases). Where fire and fragmentation do influence each other, feedback loops are possible that can lead to ecosystem conversion (e.g. forest to grassland). This is a well-documented threat in the tropics but with potential also to be important elsewhere. Fire interacts with fragmentation through scale-specific mechanisms: fire creates edges and drives edge effects; fire alters patch quality; and fire alters landscape-scale connectivity. We found only 12 cases in which studies reported the four essential strata for testing a full interaction, which were fragmented and unfragmented landscapes that both span contrasting fire histories, such as recently burnt and long unburnt vegetation. Simulation and empirical studies show that fire and fragmentation can interact synergistically, multiplicatively, antagonistically or additively. These cases highlight a key reason why understanding interactions is so important: when fire and fragmentation act together they can cause local extinctions, even when their separate effects are neutral. Whether fire–fragmentation interactions benefit or disadvantage species is often determined by the species' preferred successional stage. Adding fire to landscapes generally benefits early-successional plant and animal species, whereas it is detrimental to late-successional species. However, when fire interacts with fragmentation, the direction of effect of fire on a species could be reversed from the effect expected by successional preferences. Adding fire to fragmented landscapes can be detrimental for species that would normally co-exist with fire, because species may no longer be able to disperse to their preferred successional stage. Further, animals may be attracted to particular successional stages leading to unexpected responses to fragmentation, such as higher abundance in more isolated unburnt patches. Growing human populations and increasing resource consumption suggest that fragmentation trends will worsen over coming years. Combined with increasing alteration of fire regimes due to climate change and human-caused ignitions, interactions of fire with fragmentation are likely to become more common. Our new framework paves the way for developing a better understanding of how fire interacts with fragmentation, and for conserving biodiversity in the face of these emerging challenges.     

生境破碎化对植物-昆虫及昆虫之间相互关系的影响

生境破碎化对生物多样性和生态系统功能影响是当前国内外生态学家研究的热点问题之一。文章针对生境破碎化的内涵、量度指标进行介绍,着重分析生境破碎化对植物-昆虫关系的影响,包括植物与植食性昆虫的关系、植物与传粉昆虫的关系、种子与种子捕食者的关系,植物及其分解者的关系,还分析生境破碎化对昆虫-昆虫关系的影响,包括昆虫及其拟寄生物的关系、捕食者与猎物的关系。通过对上述方面的阐述,旨在更好地理解生境破碎化对动植物群落相互关系产生的深刻影响,并提出今后研究中应注意的问题和研究热点。     

Replication forks stalled at ultraviolet lesions are rescued via RecA and RuvABC protein-catalyzed disintegration in Escherichia coli

Ultraviolet (UV) irradiation is not known to induce chromosomal fragmentation in sublethal doses, and yet UV irradiation causes genetic instability and cancer, suggesting that chromosomes are fragmented. Here we show that UV irradiation induces fragmentation in sublethal doses, but the broken chromosomes are repaired or degraded by RecBCD; therefore, to observe full fragmentation, RecBCD enzyme needs to be inactivated. Using quantitative pulsed field gel electrophoresis and sensitive DNA synthesis measurements, we investigated the mechanisms of UV radiation-induced chromosomal fragmentation in recBC mutants, comparing five existing models of DNA damage-induced fragmentation. We found that fragmentation depends on active DNA synthesis before, but not after, UV irradiation. At low UV irradiation doses, fragmentation does not need excision repair or daughter strand gap repair. Fragmentation absolutely depends on both RecA-catalyzed homologous strand exchange and RuvABC-catalyzed Holliday junction resolution. Thus, chromosomes fragment when replication forks stall at UV lesions and regress, generating Holliday junctions. Remarkably, cells specifically utilize fork breakage to rescue stalled replication and avoid lethality.