The mid‐season crash in aphid populations: why and how does it occur?

Abstract. 1. Aphid populations on agricultural crops in temperature regions collapse over a few days from peak numbers to local extinction soon after mid‐summer (e.g. mid‐July in the U.K.). The populations recover 6–8 weeks later. There is anecdotal or incidental evidence of an equivalent mid‐season population crash of aphids on grasses and forbs in natural vegetation. 2. The ecological factors causing the mid‐season population crash of aphids include a decline in plant nutritional quality and increased natural enemy pressure as the season progresses. Extreme weather events, e.g. severe rainstorms, can precipitate the crash but weather conditions are not a consistent contributory factor. 3. The population processes underlying the crash comprise enhanced emigration, especially by alate (winged) aphids, depressed performance resulting in reduced birth rates, and elevated mortality caused by natural enemies. 4. Mathematical models, previously applied to aphid populations on agricultural crops, have great potential for studies of aphid dynamics in natural vegetation. In particular, they can help identify the contribution of various ecological factors to the timing of the population crash and offer explanations for how slow changes in population processes can result in a rapid collapse of aphid populations.     

Single-molecule biology: what is it and how does it work?

Biochemistry and structural biology are undergoing a dramatic revolution. Until now, we have tried to study subtle and complex biological processes by crude in vitro techniques, looking at average behaviors of vast numbers of molecules under conditions usually remote from those existing in the cell. Researchers have realized the limitations of this approach, but none other has been available. Now, we can not only observe the nuances of the behaviors of individual molecules but prod and probe them as well. Perhaps most important is the emerging ability to carry out such observations and manipulations within the living cell. The long-awaited leap to an in vivo biochemistry is at last underway.     

Aerobic dive limit: how often does it occur in nature?

Diving animals offer a unique opportunity to study the importance of physiological constraint in their everyday behaviors. An important component of the physiological capability of any diving animal is its aerobic dive limit (ADL). The ADL has only been measured in a few species. The goal of this study was to estimate the aerobic dive limit from measurements of body oxygen stores and at sea metabolism. This calculated ADL (cADL) was then compared to measurements of diving behavior of individual animals of three species of otariids, the Antarctic fur seal, Arctocephalus gazella, the Australian sea lion, Neophoca cinerea, and the New Zealand sea lion, Phocarctos hookeri. Antarctic fur seals dove well within the cADL. In contrast, many individuals of both sea lion species exceeded the cADL, some by significant amounts. Australian sea lions typically dove 1.4 times longer than the cADL, while New Zealand sea lions on average dove 1.5 times longer than the cADL. The tendency to exceed the cADL was correlated with the dive pattern of individual animals. In both Antarctic Fur Seals and Australian sea lions, deeper diving females made longer dives that approached or exceeded the cADL (P<0.01, r(2)=0.54). Australian and New Zealand sea lions with longer bottom times also exceeded the cADL to a greater degree. The two sea lions forage on the benthos while the fur seals feed shallow in the water column. It appears that benthic foraging requires these animals to reach or exceed their aerobic dive limit.     

Host switching in cowbird brood parasites: how often does it occur?

Avian obligate brood parasites lay their eggs in nests of host species, which provide all parental care. Brood parasites may be host specialists, if they use one or a few host species, or host generalists, if they parasitize many hosts. Within the latter, strains of host‐specific females might coexist. Although females preferentially parasitize one host, they may occasionally successfully parasitize the nest of another species. These host switching events allow the colonization of new hosts and the expansion of brood parasites into new areas. In this study, we analyse host switching in two parasitic cowbirds, the specialist screaming cowbird (Molothrus rufoaxillaris) and the generalist shiny cowbird (M. bonariensis), and compare the frequency of host switches between these species with different parasitism strategies. Contrary to expected, host switches did not occur more frequently in the generalist than in the specialist brood parasite. We also found that migration between hosts was asymmetrical in most cases and host switches towards one host were more recurrent than backwards, thus differing among hosts within the same species. This might depend on a combination of factors including the rate at which females lay eggs in nests of alternative hosts, fledging success of the chicks in this new host and their subsequent success in parasitizing it.     

Vesicular transport in capillary endothelium: does it occur?

A revised picture of the organization of endothelial plasmalemmal vesicles is presented. Three-dimensional reconstructions of endothelial segments from frog mesenteric capillaries and rat heart capillaries based on ultrathin serial sectioning have shown that plasmalemmal vesicles are not true vesicles but parts of an elaborate system of invaginations of the surface membrane. The revised picture probably applies to capillary endothelia in general. The absence of free cytoplasmic vesicles implies that vesicular transport is unlikely to occur. A reinterpretation of previous studies of vesicular transport shows that they are equally compatible with the present view that plasmalemmal vesicles are static elements of invaginations of the endothelial surface membrane.     

Apoptosis in the heart: when and why?

Since mammalian cardiac myocytes essentially rely on aerobic energy metabolism, it has been assumed that cardiocytes die in a catastrophic breakdown of cellular homeostasis (i.e. necrosis), if oxygen supply remains below a critical limit. Recent observations, however, indicate that a process of gene-directed cellular suicide (i.e. apoptosis) is activated in terminally differentiated cardiocytes of the adult mammalian heart by ischemia and reperfusion, and by cardiac overload as well. Apoptosis or programmed cell death is an actively regulated process of cellular self destruction, which requires energy and de novo gene expression, and which is directed by an inborn genetic program. The final result of this program is the fragmentation of nuclear DNA into typical nucleosomal ladders, while the functional integrity of the cell membrane and of other cellular organelles is still maintained. The critical step in this regulated apoptotic DNA fragmentation is the proteolytic inactivation of poly-[ADPribose]-polymerase (PARP) by a group of cysteine proteases with some structural homologies to interleukin-1-converting enzyme (ICE-related proteases [IRPs] such as apopain, yama and others). PARP catalyzes the ADP-ribosylation of nuclear proteins at the sites of spontaneous DNA strand breaks and thereby facilitates the repair of this DNA damage. IRP-mediated destruction of PARP, the supervisor of the genome, can be induced by activation of membrane receptors (e.g. FAS or APOI) and other signals, and is inhibited by activation of anti-death genes (e.g. bcl-2). Overload-triggered myocyte apoptosis appears to contribute to the transition to cardiac failure, which can be prevented by therapeutic hemodynamic unloading. In myocardial ischemia, the activation of the apoptotic program in cardiocytes does not exclude their final destiny to catastrophic necrosis with release of cytosolic enzymes, but might be considered as an adaptive process in hypoperfused ventricular zones, sacrificing some jeopardized myocytes to regulated apoptosis, which may by less arrhythmogenic than necrosis with the primary disturbance of membrane function.     

Symmetry breakage in the vertebrate embryo: When does it happen and how does it work?

Asymmetric development of the vertebrate embryo has fascinated embryologists for over a century. Much has been learned since the asymmetric Nodal signaling cascade in the left lateral plate mesoderm was detected, and began to be unraveled over the past decade or two. When and how symmetry is initially broken, however, has remained a matter of debate. Two essentially mutually exclusive models prevail. Cilia-driven leftward flow of extracellular fluids occurs in mammalian, fish and amphibian embryos. A great deal of experimental evidence indicates that this flow is indeed required for symmetry breaking. An alternative model has argued, however, that flow simply acts as an amplification step for early asymmetric cues generated by ion flux during the first cleavage divisions. In this review we critically evaluate the experimental basis of both models. Although a number of open questions persist, the available evidence is best compatible with flow-based symmetry breakage as the archetypical mode of symmetry breakage.     

Regeneration in the metazoans: why does it happen?

Why does regeneration occur? And why, when it manifests itself, does it do so in some but not all metazoan species? Hence, what are the permissive or inhibitory factors operating behind this phenomenon? When it comes to regeneration, many questions, such as these, remain unanswered. In fact, the problem of animal regeneration has withstood the probing of scientific inquiry for over 250 years and still awaits a satisfactory mechanistic explanation. In this essay, I will review the distribution and the modes of regeneration that are found in the different metazoan phyla. Also, I will re-examine ideas on its evolutionary origins, and discuss its possible relationship to both asexual reproduction and embryogenesis. This endeavor has two objectives. First, to bring forward an interpretation of regeneration which integrates evolutionary and developmental considerations into its discussion. And second, to suggest a comparative experimental approach to this problem that may bring us closer to understanding the molecular basis of this long-standing biological problem. BioEssays 22:578-590, 2000.     

Impact factor in cytopathology journals: what does it reflect and how much does it matter?

B. AbdullGaffar
Impact factor in cytopathology journals: what does it reflect and how much does it matter? Objective: To study the trends of impact factor (IF) in four cytopathology journals. To investigate the factors that might influence IF in cytopathology literature and whether IF has any impact on cytopathology practice. Methods: The IFs of four cytopathology journals were searched from 2005 to 2009. The IFs and their relationships with the types and number of publications, publishers, the official societies, readership, the quality of their contents, the topics covered and the levels of evidence were compared. Results: Cancer Cytopathology (CC) had the highest IF. Acta Cytologica (AC) had the lowest IF, which appeared to be in decline. Cytopathology (C) and Diagnostic Cytopathology (DC) had a slow but steady increase in their IF. Components that might influence these differences could include the category and the society of the journal, targeted readers and certain types of publications. Publishers, the number of publications, the types of topics covered and the levels of evidence probably have no major effect on IF. Conclusions: IF has its own benefits and original applications. IF is a quantitative measure that does not reflect the levels of evidence in cytopathology journals. IF should not be abandoned because it might encourage competition between cytopathology journals, but it should not dictate their contents.     

Subfunctionalization: How often does it occur? How long does it take?

The mechanisms responsible for the preservation of duplicate genes have been debated for more than 70 years. Recently, Lynch and Force have proposed a new explanation: subfunctionalization--after duplication the two gene copies specialize to perform complementary functions. We investigate the probability that subfunctionalization occurs, the amount of time after duplication that it takes for the outcome to be resolved, and the relationship of these quantities to the population size and mutation rates.     

Transdifferentiation: why and how?

Cell therapy is based on the replacement of damaged cells in order to restore injured tissues. The first consideration is that an abundant source of cells is needed; second, these cells should be immunologically compatible with the guest and third, there should be no real threat of these cells undergoing malignant transformation in the future. Given these requirements, already differentiated adult cells or adult stem cells obtained from the body of the patient appear to be the ideal candidates to meet all of these demands. The utilization of somatic cells also avoids numerous ethical and political drawbacks and concerns. Transdifferentiation is the phenomenon by which an adult differentiated cell switches to another differentiated cell. This paper reviews the importance of transdifferentiation, discussing the cells that are suitable for this process and the methods currently employed to induce the change in cell type.     

Nucleosome positioning: How is it established, and why does it matter?

Packaging of eukaryotic genomes into chromatin affects every process that occurs on DNA. The positioning of nucleosomes on underlying DNA plays a key role in the regulation of these processes, as the nucleosome occludes underlying DNA sequences. Here, we review the literature on mapping nucleosome positions in various organisms, and discuss how nucleosome positions are established, what effect nucleosome positioning has on control of gene expression, and touch on the correlations between chromatin packaging, sequence evolution, and the evolution of gene expression programs.     

Who is where in the Plastisphere,and why does it matter?

To fully understand how plastic is affecting the ocean, we need to understand how marine life interacts directly with it. Besides their ecological relevance, microbes can affect the distribution, degradation and transfer of plastics to the rest of the marine food web. From amplicon sequencing and scanning electron microscopy, we know that a diverse array of microorganisms rapidly associate with plastic marine debris in the form of biofouling and biofilms, also known as the “Plastisphere.” However, observation of multiple microbial interactions in situ, at small spatial scales in the Plastisphere, has been a challenge. In this issue of Molecular Ecology Resources, Schlundt et al. apply the combination labelling and spectral imaging – fluorescence in situ hybridization to study microbial communities on plastic marine debris. The images demonstrate the colocalization of abundant bacterial groups on plastic marine debris at a relatively high taxonomic and spatial resolution while also visualizing biofouling of eukaryotes, such as diatoms and bryozoans. This modern imaging technology provides new possibilities to address questions regarding the ecology of marine microbes on plastic marine debris and describe more specific impacts of plastic pollution in the marine food webs.     

Nitrogen limitation on land: how can it occur in Earth system models?

The representation of the nitrogen (N) cycle in Earth system models (ESMs) is strongly motivated by the constraint N poses on the sequestration of anthropogenic carbon (C). Models typically implement a stoichiometric relationship between C and N in which external supply and assimilation by organisms are adjusted to maintain their internal stoichiometry. N limitation of primary productivity thus occurs if the N supply from uptake and fixation cannot keep up with the construction of tissues allowed by C assimilation. This basic approach, however, presents considerable challenges in how to faithfully represent N limitation. Here, we review how N limitation is currently implemented and evaluated in ESMs and highlight challenges and opportunities in their future development. At or near steady state, N limitation is governed by the magnitude of losses from the plant‐unavailable pool vs. N fixation and there are considerable differences in how models treat both processes. In nonsteady‐state systems, the accumulation of N in pools with slow turnover rates reduces N available for plant uptake and can be challenging to represent when initializing ESM simulations. Transactional N limitation occurs when N is incorporated into various vegetation and soil pools and becomes available to plants only after it is mineralized, the dynamics of which depends on how ESMs represent decomposition processes in soils. Other challenges for ESMs emerge when considering seasonal to interannual climatic oscillations as they create asynchronies between C and N demand, leading to transient alternations between N surplus and deficit. Proper evaluation of N dynamics in ESMs requires conceptual understanding of the main levers that trigger N limitation, and we highlight key measurements and observations that can help constrain these levers. Two of the biggest challenges are the mechanistic representation of plant controls on N availability and turnover, including N fixation and organic matter decomposition processes.     

Cell-cycle-specific Golgi fragmentation: how and why?

The Golgi membranes, in the form of stacks of cisternae, are contained in the pericentriolar region of mammalian cells. During mitosis, these membranes are fragmented and dispersed throughout the cell. Recent studies are revealing the significance of pericentriolar position of the Golgi apparatus and mechanism by which these membranes are fragmented during mitosis.     

What is MRI bone oedema in rheumatoid arthritis and why does it matter?

MRI bone oedema occurs in various forms of inflammatory and non-inflammatory arthritis and probably represents a cellular infiltrate within bone. It is common in early rheumatoid arthritis and is associated with erosive progression and poor functional outcome. Histopathological studies suggest that a cellular infiltrate comprising lymphocytes and osteoclasts may be detected in subchondral bone and could mediate the development of erosions from the marrow towards the joint surface. There is emerging evidence from animal models that such an infiltrate corresponds with MRI bone oedema, pointing towards the bone marrow as a site for important pathology driving joint damage in rheumatoid arthritis.