The ethics of functional genomics: same, same, but different?

Respect for human life--a notion of worth uniting all members of the human race--constitutes a sense of anthropocentrism that has long been the justification for the enrollment of animals in experimentation executed to develop therapies to alleviate human suffering. Currently, however, advances in functional genomics are causing a qualitative transformation of the rationale for medical research performed on animals. The notion of human distinctness is being fundamentally challenged when gene sequences similar to those found in humans are identified in different species. In this Opinion article, we would like to highlight an inherent tension brought about by the current developments in functional genomics: a tension between the scientific and the ethical status of gene sequences. Is it reasonable to argue that they are the same for all practical purposes but different in ethical status?     

Does foliage on the same branch compete for the same water? Experiments on Douglas-fir trees

Do branchlets within a branch have autonomous water supplies, or do they share a common water supply system? We hypothesized that if branchlets shared a common water supply, then stomatal conductance (g_s) on sunlit foliage would increase with reduced transpiration of competing foliage on the branch. We reduced transpiration of other foliage on the branch through bagging and shading, and we monitored the gas-exchange responses of the remaining sunlit foliage on the branch relative to control branches for several age classes of Douglas-fir trees (aged ~10 years, 20 years, and 450 years old). Contrary to our hypothesis, we found no increases in g_s in either young or old trees following transient reductions in the amount of transpiring leaf area. The diurnal change in water potential, mid-day stomatal closure and associated photosynthetic decline occurred at the same time and were of the same magnitude on both treated and untreated branches, with the exception of photosynthesis in one 450-year-old tree. Hydraulic conductance measurements of branch junctions indicate that xylem within branches is only partially interconnected which would reduce the effectiveness of shading as a means of increasing water supply to the remaining sunlit foliage. The lack of a response implies that when a branch is in partial shade, the remaining sunlit foliage has no advantage with respect to water status over foliage on a branch completely in the sun.     

Viruses and autoimmune disease--two sides of the same coin?

Some viruses have the ability to modulate the development of autoimmune diseases. Virus infections have long been associated with the exacerbation of autoimmune disease, however, there is also evidence that viruses can actually protect against autoimmune disease. Several experimental models have been developed to investigate how some virus infections can prime for and trigger autoimmunity whereas others ameliorate the pathway leading to clinical disease. It is possible that the type I interferons, via interleukin 12, provide the link between viruses and autoimmunity.     

Native and alien invasive plants: more of the same?

We compare the ecological and habitat characteristics of alien and native vascular plants which have recently expanded in range m England, Scotland, the Republic of Ireland and the Netherlands In the great majority of respects, expanding aliens and natives are functionally indistinguishable However, there are a few consistent differences aliens are more likely than natives to be clonal, polycarpic perennials with erect, leafy stems, and to have transient seed banks We discuss these trends m the context of the difficulties faced by aliens in invading mostly closed plant communities in relatively cool, damp climates Our results are consistent with some predictions of the attributes of'ideal'invaders, but contradict others We argue that the ecological attributes of successful alien invaders are strongly habitat-dependent     

Pollination and stigma wounding: same response, different signal?

In Petunia hybrida flowers, both pollination and stigma woundinginduced a transient Increase in ethylene production and hastenedcorolla senescence. Ethylene production by different flowerparts was measured in situ using laser photoacoustic (LPA) spectroscopy.In pollinated flowers, ethylene was exclusively produced bythe stigma/style region whereas wounding of the stigma Inducedethylene production both by the stigma/style region and by theremaining flower parts. In aminoethoxyvinylglycine (AVG)-treatedflowers, subsequent treatment of the unwounded stigma with 1-aminocyclopropane-1-carboxylicacid (ACC) induced ethylene production exclusively by the stigma/styleregion whereas treatment of a previously wounded stigma withACC induced a simultaneous increase in ethylene production bythe stigma/style region and the remaining flower parts. Theseresults suggest that following stigma wounding, either ACC orethylene is involved in inter-organ communication. Followingpollination, the signal is apparently not directly related toethylene. In vivo ACC oxidase activity of most flower parts, includingthe gynoecium, was higher in light than in dark. Light or darkdid not influence the relative contributions of stigma/styleand remaining flower parts to the total pollination, woundingor ACC-induced ethylene production, indicating that ACC is nottranslocated. Both in excised styles and intact flowers, radiolabelledACC and its analogue -aminoisobutyric acid (AIB), applied eitherto an intact or wounded stigma, were largely immobile confirmingthat ACC is not likely to play a role in inter-organ signalling. The results collectively suggest that following stigma wounding,translocation of ethylene may be the signal responsible forinitiation of corolla senescence; following pollination thesignal is not directly related to ethylene. Key words: 1-Aminocyclopropane-1-carboxylic acid (ACC), ethylene, flower senescence, Petunia hybrida, pollination, stigma wounding     

The neuronal ceroid lipofuscinoses: the same, but different?

The NCLs (neuronal ceroid lipofuscinoses) (also known as Batten disease) are a group of at least ten fatal inherited storage disorders. Despite the identification of many of the disease-causing genes, very little is known about the underlying disease mechanisms. However, now that we have mouse or large-animal models for most forms of NCL, we can investigate pathogenesis and compare what happens in the brain in different types of the disease. Broadly similar neuropathological themes have emerged, including the highly selective nature of neuron loss, early effects upon the presynaptic compartment, together with an early and localized glial activation. These events are especially pronounced within the thalamocortical system, but it is clear that where and when they occur varies markedly between different forms of NCL. It is now becoming apparent that, despite having pathological endpoints that resemble one another, these are reached by a sequence of events that is specific to each subtype of NCL.     

Malaria and trypanosome transmission: different parasites, same rules?

African trypanosomes produce different specialized stages for within-host replication and between-host transmission and therefore face a resource allocation trade-off between maintaining the current infection (survival) and investment into transmission (reproduction). Evolutionary theory predicts the resolution of this trade-off will significantly affect virulence and infectiousness. The application of life history theory to malaria parasites has provided novel insight into their strategies for survival and reproduction; how this framework can now be applied to trypanosomes is discussed. Specifically, predictions for how parasites trade-off investment in survival and transmission in response to variation in the within-host environment are outlined. An evolutionary approach has the power to explain why patterns of investment vary between strains and during infections, giving important insights into parasite biology.     

Tumorigenesis and neurodegeneration: two sides of the same coin?

Dysregulation of genes that control cell-cycle progression and DNA repair is a hallmark of tumorigenesis. It is becoming increasingly apparent, however, that these defects also contribute to degeneration of post-mitotic neurons under certain conditions. The gene for ataxia-telangiectasia mutated (ATM) is a prototype for this dual mechanism of action, with loss-of-function mutations causing not only selective degeneration of cerebellar neurons but also increased susceptibility to breast cancer and hematologic malignancy. Increased dosage of amyloid precursor protein in Down syndrome (trisomy 21) predisposes to dementia of Alzheimer type and may also contribute to acute leukemia and transient myeloproliferative disorder. The gene parkin, loss-of-function mutations in which account for about half of cases of early-onset Parkinson disease, has been identified as a candidate tumor suppressor gene by several groups. Parkin is deleted or downregulated in several tumor types, and its re-expression sensitizes derivative cell lines to inhibitors of cell-cycle progression. The overlap of molecular pathways implicated in cancer and neurodegeneration challenges long-held notions about differentiated cellular states and may open the door to novel therapeutic approaches to both groups of disorders.     

Do stress and long-term potentiation share the same molecular mechanisms?

Stress is a biological, significant factor shown to influence hippocampal synaptic plasticity and cognitive functions. Although numerous studies have reported that stress produces a suppression in long-term potentiation (LTP; a putative synaptic mechanism underlying learning and memory), little is known about the mechanism by which this occurs. Because the effects of stress on LTP and its converse process, long-term depression (LTD), parallel the changes in synapticity that occur following the establishment of LTP with tetanic stimulation (i.e., occluding LTP and enhancing LTD induction), it has been proposed that stress affects subsequent hippocampal plasticity by sharing the same molecular machinery required to support LTP. This article summarizes recent findings from ours and other laboratories to assess this view and discusses relevant hypotheses in the study of stress-related modifications of synaptic plasticity.     

Animal models of PD: pieces of the same puzzle?

Parkinson's disease (PD) is a common neurodegenerative disorder with no known cure. The etiology of PD is likely due, in part, to combinations of genetic susceptibilities and environmental factors. In rare familial cases, PD is due to genetic mutations. A number of new genetic and toxin models of PD and advances in older models are yielding important new information about the pathogenesis of PD. This has prompted us to critically review the current animal models for PD and discuss how these models may yield fresh insights into the pathogenesis of PD, as well as new therapeutic opportunities.     

Lab and field experiments: Are they the same animal?

To advance our understanding of biological processes we often plan our experiments based on published data. This can be confusing though, as data from experiments performed in a laboratory environment are sometimes different from, or completely opposite to, findings from similar experiments performed in the “real world”. In this mini-review, we discuss instances where results from laboratory experiments differ as a result of laboratory housing conditions, and where they differ from results gathered in the field environment. Experiments involving endocrinology and behavior appear to be particularly susceptible to influence from the environment in which they are performed.As such, we have attempted to promote discussion of the influence of housing environment on the reproductive axis, circadian biology and behavior, immune function, stress biology, neuroplasticity and photoperiodism. For example, why should a rodent species be diurnal in one housing environment yet nocturnal in another? Are data that are gathered from experiments in the laboratory applicable to the field environment, and vice-versa? We hope not only to highlight the need for experiments in both lab and field when looking at complex biological systems, but also to promote frank discussion of discordant data. Perhaps, just as study of individual variation has been gaining momentum in recent years, data from variation between experimental arenas can provide us with novel lines of research.     

Epigenetics: imprinting in plants and mammals--the same but different?

Plants and animals both exhibit parental imprinting, but do they control it the same way? Recent studies show that in Arabidopsis, as in mammals, imprinted alleles are subject to DNA methylation--but, surprisingly, the default state is silence rather than activity.