|
ScienceWeek
SCIENCEWEEK
September 8, 2007
Vol. 11 - Number 35
--------------------------------
What would have happened if Darwin and Einstein as young men had needed to apply for government support? Their probability of getting past the grant reviewers would be similar to a snowball surviving in Hell.
-- Craig Loehle
--------------------------------
Contents (full text below):
1. Animal Behavior: Chimpanzees and Punitive Behavior
2. Medical Biology: On Parkinson's Disease
=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=
1.
Proc. Nat. Acad. Sci. | August 21, 2007 | vol. 104 | no. 34 | 13537-13538
Animal Behavior: Chimpanzees and Punitive Behavior
Joan B. Silk
Humans are the most cooperative species on the planet, and the most punitive. This is no coincidence. When I promise to take a friend to the airport to catch an early-morning flight, I have to overcome the temptation to sleep an extra couple of hours. My motivation to follow through on my promise is influenced by my awareness of the consequences: my friend will miss her plane, and I will feel guilty. My friend will probably be angry with me, and she may refuse to help me the next time I ask. Worse yet, she may tell other people what I did, and they may share her outrage and anger. The threat of these kinds of sanctions helps to sustain cooperation within dyads and larger groups (1–4). There is now considerable interest in the evolution of cooperation and punishment in human societies, and there have been a number of efforts to explore the phylogenetic origins of cooperative motives in other primates (4–8). Virtually all of the work on other primates has focused on the willingness to provide benefits to conspecifics. In this issue, Jensen et al. (9) turn the tables and examine chimpanzees' propensity to impose sanctions on familiar group members who commit transgressions.
To study chimpanzees' propensity for punitive behavior, Jensen et al. (9) devised an ingenious experimental protocol in which one chimpanzee was given the opportunity to respond to the loss or inaccessibility of valued food items by pulling a rope that caused a platform to collapse and the food to fall out of reach. This setup allowed the researchers to examine how chimpanzees responded when food was inaccessible or taken away from them, how they responded to disparities in outcomes between themselves and others, and their sensitivity to the role others played in their losses.
In the first experiment, Jensen et al. (9) compared the chimpanzees' responses to variation in the accessibility and desirability of rewards. Sensibly enough, chimpanzees were more likely to pull the rope and dump the items on the floor when they were given access to inedible pieces of plastic and bamboo than when they were given access to tasty items. Similarly, they were more likely to collapse the table when food was inaccessible to them than when it was placed within reach. So far, there is nothing particularly social about the chimpanzees' responses: when they are unable to obtain access to food, they are likely to pull the rope and collapse the table. The key finding from this experiment is that the chimpanzees were as likely to collapse the table when another chimpanzee had access to the food as when no one had access to the food. Thus, chimpanzees do not seem to retaliate against other chimpanzees simply for getting lucky.
In a second experiment, the researchers explored the chimpanzees' sensitivity to the nature of losses that they suffered. In this experiment, food was placed on a sliding platform that could be moved out of the actor's reach. As before, the actor could pull a rope that caused the platform to collapse and the food to fall. In one condition, a human experimenter moved the platform away from the actor and slid it to within reach of another chimpanzee. In another condition, the experimenter did the same thing, but there was no other chimpanzee present to receive the food. In the last condition, a chimpanzee in the opposite cage was able to pull the platform away from the actor and gain access to the food. Not surprisingly, the chimpanzees were more likely to collapse the table when they lost food than when they were left alone to eat in peace. However, the chimpanzees were significantly more likely to respond punitively when they were victimized by other chimpanzees than when they were the victims of the experimenter's whims.
=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=
2.
PNAS | July 17, 2007 | vol. 104 | no. 29 | 11867-11868
Medical Biology: On Parkinson's Disease
Ken Nakamura and Robert H. Edwards
Over the last few years, human genetics has provided a series of invaluable entry points to understanding the pathogenesis of Parkinson's disease (PD). Relative to dominantly inherited forms of PD caused by mutations in the proteins {alpha}-synuclein and leucine-rich repeat kinase 2 (LRRK2), recessive forms of PD do not seem to bear as close a resemblance to the sporadic disorder. Mutations in parkin produce a distinctive, early onset clinical syndrome with slower progression than the idiopathic disorder (1). Parkin functions as an E3 ubiquitin ligase, suggesting a role in targeting to the proteasome and protein turnover. Considering this biochemical activity, it is surprising that the pathology associated with mutations in parkin shows no Lewy bodies or obvious protein deposits. Indeed, ubiquitination by parkin may control other cellular processes such as endocytosis (2). Nonetheless, mutations in parkin do result in the loss of midbrain dopamine neurons. Mutations in the protein DJ-1 implicated in the response to oxidative stress also produce recessive parkinsonism (3, 4), but there is very little if any pathology available. Although the condition responds to dopamine replacement therapy, we do not know whether it actually involves a loss of dopamine neurons. Similarly, mutations in the PTEN-induced putative kinase 1 (PINK1), the subject of the paper by Kitada et al. in a recent issue of PNAS (5), cause a form of recessive parkinsonism (6), but its pathological basis also remains to be characterized. Nonetheless, a significant number of patients with later-onset parkinsonism that strongly resembles idiopathic PD have heterozygous, or occasionally homozygous, mutations in parkin, DJ-1, and PINK1 (7), supporting their relationship to the sporadic disorder.
The analysis of recessive parkinsonism has the advantage that it focuses on the loss of a normal function rather than on the gain of an abnormal function, which can be difficult to reproduce and understand. A number of groups therefore have disrupted the genes encoding parkin and DJ-1 in mice and other model organisms. Despite its predicted role in protein degradation, the loss of parkin in mice does not result in protein deposition or the degeneration of dopamine neurons (8, 9). On the other hand, parkin knockout mice do show physiological and behavioral deficits attributable to the nigrostriatal dopamine system (8), raising the possibility that these deficits somehow predispose to the degeneration observed in patients or at least result from the same pathogenic process. Similarly, the loss of DJ-1 in mice impairs dopamine release in the striatum, but without any reduction in the number of dopamine neurons, even in aged animals (10, 11). Because we know little about the pathology of DJ-1-associated PD, it remains possible that the knockout mouse may accurately model the human condition. Alternatively, defects in dopamine release may somehow predispose to dopamine cell degeneration in this case as well. Indeed, DJ-1-deficient animals are more sensitive to a number of neurotoxins (12–14), but again we do not know whether this results from a defect in dopamine release or is an independent consequence of DJ-1 loss.
Recessive parkinsonism has proven to be particularly amenable to genetic analysis in Drosophila melanogaster. Loss of parkin in Drosophila produces severe mitochondrial abnormalities in the male germ line and in flight muscle, accompanied by degeneration that also may affect some of the dopamine neurons (15). Although parkin knockout mice show no degeneration of dopamine neurons or mitochondrial pathology, they do appear to exhibit a functional deficit in the respiratory chain (16). The identification of mitochondrial abnormalities is particularly significant because the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) still provides what is in many ways the best animal model for PD and involves the inhibition of mitochondrial complex I (17). The high energy demands of flight muscle presumably make this tissue particularly vulnerable to a disturbance in oxidative phosphorylation.
The analysis of PINK1 has further supported a role for mitochondria in the pathogenesis of PD. First, PINK1 is a mitochondrially targeted kinase (6). Second, mutations in Drosophila PINK1 produce mitochondrial abnormalities very similar to those observed with mutations in parkin (18, 19). Further, the overexpression of parkin suppresses the effect of mutations in PINK1, indicating that parkin acts downstream of PINK1 in the same pathway.
=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=
|