The power of the weak: When altruism is the equilibrium.

A rational economic analysis complements Grossmann's fearful ape hypothesis. Two examples of mixed-motive games with strong inter-dependence (i.e., weak chirping nestling, boxed pigs) demonstrate that signaling weakness is a dominant strategy. Weakness elicits cooperative, caring response, comprising the equilibrium of the game. In extensive form, a reliable reputation of weakness elicits caring as a sequential equilibrium.

Frequency of enforcement is more important than the severity of punishment in reducing violation behaviors.

External enforcement policies aimed to reduce violations differ on two key components: the probability of inspection and the severity of the punishment. Different lines of research offer different insights regarding the relative importance of each component. In four studies, students and Prolific crowdsourcing participants (Ntotal = 816) repeatedly faced temptations to commit violations under two enforcement policies. Controlling for expected value, we found that a policy combining a high probability of inspection with a low severity of fines (HILS) was more effective than an economically equivalent policy that combined a low probability of inspection with a high severity of fines (LIHS). The advantage of prioritizing inspection frequency over punishment severity (HILS over LIHS) was greater for participants who, in the absence of enforcement, started out with a higher violation rate. Consistent with studies of decisions from experience, frequent enforcement with small fines was more effective than rare severe fines even when we announced the severity of the fine in advance to boost deterrence. In addition, in line with the phenomenon of underweighting of rare events, the effect was stronger when the probability of inspection was rarer (as in most real-life inspection probabilities) and was eliminated under moderate inspection probabilities. We thus recommend that policymakers looking to effectively reduce recurring violations among noncriminal populations should consider increasing inspection rates rather than punishment severity.

One-by-One or All-at-Once? Self-Reporting Policies and Dishonesty.

Organizational monitoring relies frequently on self-reports (e.g., work hours, progress reports, travel expenses). A "one-by-one" policy requires employees to submit a series of reports (e.g., daily or itemized reports). An "all-at-once" policy requires an overall report (e.g., an annual or an overview report). Both policies use people's self-reports to determine their pay, and both allow people to inflate their reports to get higher incentives, that is, to cheat. Objectively, people can cheat to the same extent under both reporting policies. However, the two policies differ in that the segmented one-by-one policy signals closer monitoring than the all-at-once policy. We suggest here that lie aversion may have a paradoxical effect on closer monitoring and lead people to cheat more. Specifically, reporting a series of segmented units of performance (allowing small lies) should lead to more cheating than a one-shot report of overall performance (that require one larger lie). Two surveys indicated that while people perceive the all-at-once policy as more trusting, they still expected people would be equally likely to cheat in both policies. An experiment tested the effects of the two reporting policies on cheating. The findings showed that contrary to the participants' intuition, but in line with research on lie aversion, the one-by-one policy resulted in more cheating than the all-at-once policy. Implications for future research and organization policy are discussed.

Three Principles to REVISE People's Unethical Behavior.

Dishonesty and unethical behavior are widespread in the public and private sectors and cause immense annual losses. For instance, estimates of U.S. annual losses indicate $1 trillion paid in bribes, $270 billion lost due to unreported income, and $42 billion lost in retail due to shoplifting and employee theft. In this article, we draw on insights from the growing fields of moral psychology and behavioral ethics to present a three-principle framework we call REVISE. This framework classifies forces that affect dishonesty into three main categories and then redirects those forces to encourage moral behavior. The first principle, reminding, emphasizes the effectiveness of subtle cues that increase the salience of morality and decrease people's ability to justify dishonesty. The second principle, visibility, aims to restrict anonymity, prompt peer monitoring, and elicit responsible norms. The third principle, self-engagement, increases people's motivation to maintain a positive self-perception as a moral person and helps bridge the gap between moral values and actual behavior. The REVISE framework can guide the design of policy interventions to defeat dishonesty.

Hutchinson-Gilford progeria syndrome through the lens of transcription.

Lamins are nuclear intermediate filaments. In addition to their structural roles, they are implicated in basic nuclear functions such as chromatin organization, DNA replication, transcription, DNA repair, and cell-cycle progression. Mutations in human LMNA gene cause several diseases termed laminopathies. One of the laminopathic diseases is Hutchinson-Gilford progeria syndrome (HGPS), which is caused by a spontaneous mutation and characterized by premature aging. HGPS phenotypes share certain similarities with several apparently comparable medical conditions, such as aging and atherosclerosis, with the conspicuous absence of neuronal degeneration and cancer rarity during the short lifespan of the patients. Cell lines from HGPS patients are characterized by multiple nuclear defects, which include abnormal morphology, altered histone modification patterns, and increased DNA damage. These cell lines provide insight into the molecular pathways including senescence that require lamins A and B1. Here, we review recent data on HGPS phenotypes through the lens of transcriptional deregulation caused by lack of functional lamin A, progerin accumulation, and lamin B1 silencing.

The pot calling the kettle black: distancing response to ethical dissonance.

Six studies demonstrate the "pot calling the kettle black" phenomenon whereby people are guilty of the very fault they identify in others. Recalling an undeniable ethical failure, people experience ethical dissonance between their moral values and their behavioral misconduct. Our findings indicate that to reduce ethical dissonance, individuals use a double-distancing mechanism. Using an overcompensating ethical code, they judge others more harshly and present themselves as more virtuous and ethical (Studies 1, 2, 3). We show this mechanism is exclusive for ethical dissonance and is not triggered by salience of ethicality (Study 4), general sense of personal failure, or ethically neutral cognitive dissonance (Study 5). Finally, it is characterized by some boundary conditions (Study 6). We discuss the theoretical contribution of this work to research on moral regulation and ethical behavior.

Idealistic advice and pragmatic choice: a psychological distance account.

In 6 studies, we found that advice is more idealistic than choice in decisions that trade off idealistic and pragmatic considerations. We propose that because advisers are more psychologically distant from the choosers' decision problem, they construe the dilemma at a higher construal level than do choosers (Trope & Liberman, 2003, 2010). Consequently, advisers are more influenced by idealistic considerations that are salient at a high-level construal, whereas choosers are more influenced by pragmatic considerations that are salient at a low-level construal. Consistent with this view, Studies 1 and 2 demonstrate that compared with choosers, advisers weigh idealistic considerations more heavily and pragmatic considerations less heavily, place greater emphasis on ends (why) than on means to achieve the end (how), and generate more reasons (pros) in favor of acting idealistically. Studies 3 and 4 provide converging support for our account by demonstrating that making advisers focus on a lower construal level results in more pragmatic recommendations. In Study 3, we manufactured more pragmatic recommendations by priming a low-level implementation mind-set in a purportedly unrelated task, whereas in Study 4 we did so by reducing advisers' psychological distance from the dilemma by asking them to consider what they would choose in the situation. The results of Study 4 suggest advisers do not spontaneously consider self-choice. Finally, in Studies 5 and 6, we demonstrate the choice-advice difference in consequential real-life decisions.

Ce-emerin and LEM-2: essential roles in Caenorhabditis elegans development, muscle function, and mitosis.

Emerin and LEM2 are ubiquitous inner nuclear membrane proteins conserved from humans to Caenorhabditis elegans. Loss of human emerin causes Emery-Dreifuss muscular dystrophy (EDMD). To test the roles of emerin and LEM2 in somatic cells, we used null alleles of both genes to generate C. elegans animals that were either hypomorphic (LEM-2-null and heterozygous for Ce-emerin) or null for both proteins. Single-null and hypomorphic animals were viable and fertile. Double-null animals used the maternal pool of Ce-emerin to develop to the larval L2 stage, then arrested. Nondividing somatic cell nuclei appeared normal, whereas dividing cells had abnormal nuclear envelope and chromatin organization and severe defects in postembryonic cell divisions, including the mesodermal lineage. Life span was unaffected by loss of Ce-emerin alone but was significantly reduced in LEM-2-null animals, and double-null animals had an even shorter life span. In addition to striated muscle defects, double-null animals and LEM-2-null animals showed unexpected defects in smooth muscle activity. These findings implicate human LEM2 mutations as a potential cause of EDMD and further suggest human LEM2 mutations might cause distinct disorders of greater severity, since C. elegans lacking only LEM-2 had significantly reduced life span and smooth muscle activity.

A laminopathic mutation disrupting lamin filament assembly causes disease-like phenotypes in Caenorhabditis elegans.

Mutations in the human LMNA gene underlie many laminopathic diseases, including Emery-Dreifuss muscular dystrophy (EDMD); however, a mechanistic link between the effect of mutations on lamin filament assembly and disease phenotypes has not been established. We studied the ΔK46 Caenorhabditis elegans lamin mutant, corresponding to EDMD-linked ΔK32 in human lamins A and C. Cryo-electron tomography of lamin ΔK46 filaments in vitro revealed alterations in the lateral assembly of dimeric head-to-tail polymers, which causes abnormal organization of tetrameric protofilaments. Green fluorescent protein (GFP):ΔK46 lamin expressed in C. elegans was found in nuclear aggregates in postembryonic stages along with LEM-2. GFP:ΔK46 also caused mislocalization of emerin away from the nuclear periphery, consistent with a decreased ability of purified emerin to associate with lamin ΔK46 filaments in vitro. GFP:ΔK46 animals had motility defects and muscle structure abnormalities. These results show that changes in lamin filament structure can translate into disease-like phenotypes via altering the localization of nuclear lamina proteins, and suggest a model for how the ΔK32 lamin mutation may cause EDMD in humans.

Nuclear lamins: key regulators of nuclear structure and activities.

The nuclear lamina is a proteinaceous structure located underneath the inner nuclear membrane (INM), where it associates with the peripheral chromatin. It contains lamins and lamin-associated proteins, including many integral proteins of the INM, chromatin modifying proteins, transcriptional repressors and structural proteins. A fraction of lamins is also present in the nucleoplasm, where it forms stable complexes and is associated with specific nucleoplasmic proteins. The lamins and their associated proteins are required for most nuclear activities, mitosis and for linking the nucleoplasm to all major cytoskeletal networks in the cytoplasm. Mutations in nuclear lamins and their associated proteins cause about 20 different diseases that are collectively called laminopathies'. This review concentrates mainly on lamins, their structure and their roles in DNA replication, chromatin organization, adult stem cell differentiation, aging, tumorogenesis and the lamin mutations leading to laminopathic diseases.

Contrast effects or loss aversion? Comment on Usher and McClelland (2004).

M. Usher and J. L. McClelland (2004) recently proposed a new connectionist type of model to explain context effects on preferential choice including the similarity, attraction, and compromise effects. They compared their model with an earlier connectionist type model for these same effects proposed by R. Roe, J. R. Busemeyer, and J. T. Townsend (2001) and raised several new issues. The authors address these issues and point out the main theoretical differences between the 2 explanations for context effects.