Psychology

Genetics of Aggression

The genetics of aggression refers to the study of how genetic factors influence aggressive behavior. Research in this area explores the role of specific genes and genetic variations in predisposing individuals to aggressive tendencies. By examining the genetic underpinnings of aggression, scientists aim to better understand the complex interplay between genetic and environmental influences on aggressive behavior.

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12 Key excerpts on "Genetics of Aggression"

  • Book cover image for: Biological Psychiatry
    It should be admitted at the outset that even focusing on particular expressions of aggression, such as assault, homicide, or rape, does not lead to simple associations with biological factors. This review broadly looks at some of the more recent writings on the role(s) of biological factors in aggression with the intention of illustrating the modem approaches and concerns. AGGRESSION AND GENES Behavior genetics (e.g., Royce and Mos, 1979) is currently a growth area of research. In spite of the public misconception that scientists are looking for the gene involved in aggression, it is obvious that genes interact, influence developing ana-tomical and physiological systems, and are involved in interplay with the environ-ment. For many years, people have been intrigued about suggestions of links between genetic endowment and human hostility (e.g., Christiansen, 1968; Owen, 1972; Cadaret, 1978; Gottesman et al., 1983; Mednick et a1.,1987). This area has been recently substantially reviewed and re-evaluated by Carey (1994) and a Sym-posium on Genetics of Criminal and Antisocial Behaviour (edited by Bock and Goode, 1996). Carey (1994) concludes that there is a trend in most studies (of vio-lence and human genetics), albeit not always a statistically significant one, consis-tent with the hypothesis of a genetic effect on adult and perhaps adolescent anti-social behaviour. (p. 42). He points out, however, that it is not easy to integrate this literature into contemporary criminological research on violence in the U.S. In addition, the genetics of antisocial behavior do not fit any simple additive model. Carey (1994) points out that the joint effects of marital assortment, temporal trends over time, nonadditive genetic variance, special twin effects, etc., must be considered in studying the genetics of antisocial behaviour (p. 42). The evidence for a genetic effect primarily on offenses involving physical aggression is not impressive.
  • Book cover image for: The Social Psychology of Aggression
    Available until 4 Dec |Learn more
    • Barbara Krahé(Author)
    • 2020(Publication Date)
    • Routledge
      (Publisher)
    On balance, the available evidence suggests that genetic make-up must be regarded as an important source of individual variation in aggression. A precise assessment of the magnitude of its impact relative to environmental influences is difficult, hampered by various methodological problems that have been noted throughout the literature (Tedeschi & Felson, 1994). For example, studies analysing genetic vs. environmental influences on criminality often failed to distinguish between violent and non-violent crimes. This distinction is crucial if the aim is to determine the heritability of aggressive behaviour in particular, rather than antisocial or deviant behaviour in general (Burt, 2009). Furthermore, studies combining both self-report and observation are needed to resolve the issue of why the two types of measures produce diverging evidence on the strength of genetic influences.
    With regard to the question of whether or not aggression is an inevitable part of human nature and individual character, research showing the impact of genetic factors has sometimes been construed as suggesting a deterministic, and thus pessimistic, view – if individuals carry the aggressive genes, they will grow up to be aggressive. However, such a view is rejected by behaviour geneticists. They stress that individuals’ genetic make-up may predispose them towards becoming an aggressive person, but environmental factors play a crucial role in determining whether or not that predisposition will actually be expressed in aggressive behaviour. As noted by Van Goozen, Fairchild, Snoek, and Harold (2007), a genetic disposition towards aggressive behaviour may become manifested in behaviour in a negative family environment, or it may be suppressed in a positive environment. As children inherit the genetic disposition towards aggression from their parents, they are likely to grow up in a more aggression-prone family environment (Moffitt, 1993). To complicate matters further, children with a genetic disposition towards aggression may elicit negative responses from their social environment through their aggressive behaviour, also pointing to the interactive influences of nature and nurture.
    The critical role of environmental factors is also demonstrated by evidence from the field of epigenetics . This research has shown that adverse experiences affecting individuals at sensitive periods of life, especially in prenatal development and early infancy, may trigger changes in the function of genes that lead to cognitive and emotional deficits involved in aggressive behaviour (Palumbo, Mariotti, Iofrida, & Pellegrini, 2018; Waltes et al., 2016). These findings show that genetic (inherited) and environmental (acquired) factors mutually influence each other, which may explain why individual differences in aggressive behaviour are highly stable over time. We will return to the issue of stability in more detail in Chapter 4
  • Book cover image for: Social Psychology
    • Saba Safdar, Catherine A. Sanderson(Authors)
    • 2021(Publication Date)
    • Wiley
      (Publisher)
    Other evidence that suggests the role of genetics in predicting aggressive behaviour comes from longitudinal research indicating that children who are highly aggressive early in life are more likely to be aggressive later. For example, men and women with high-level childhood adversity were asso- ciated with increased risk of perpetrating compared to increased risk among men and women with low-level adversity (Roberts, McLaughlin, Conron, & Koenen, 2011). In one study of twins, over 750 participants at two age points, age 9 to 10 and 14 to 15 years, were examined (Niv, Tuvblad, Raine, & Baker, 2013). Participants were gathered from Los Angeles where their accompanying parent participated in daylong clinical interviewing and answering questionnaires that were aimed at assessing home and school environment, behaviour, personality, and psychopathol- ogy of both twins as well as of the parent. This study examined the structure of genetic and environ- mental influences on aggression and rule-breaking in order to examine change and stability across the span of childhood to mid-adolescence. Aggression and rule-breaking were found to be influenced by a latent common factor of antisocial behavior (ASB) within each wave of data collection. The variance in the childhood-age common factor of ASB was influenced by 41 percent genetics, 40 percent shared environment, and 19 percent non-shared environment. In adolescence, 41 percent of variance in the common factor were genetic, while both shared and non-shared environments remained stable over time. Additionally, both aggression and rule-breaking within each wave were found to have unique influences not common across subscales or across waves, highlighting specificity of genetic and envi- ronmental effects on different problem behaviours at both ages (Niv et al., 2013).
  • Book cover image for: Genetics of Criminal and Antisocial Behaviour
    • Gregory R. Bock, Jamie A. Goode, Gregory R. Bock, Jamie A. Goode(Authors)
    • 2008(Publication Date)
    • Wiley
      (Publisher)
    This is part of a broader picture which indicates that time and timing are crucial to understanding the relations between genetic manipulations, aggressive behaviours and development. Third, the effects of genetic background inevitably interact with experiences and other social and organismic events. These detailed studies of behaviour have permitted researchers to provide a preliminary account of the neuro- biological and endocrinological mediators for experience and genetic manipulations. Such interactions, described systematically, are required to account for observed variance in aggressive behaviour. The resultant model can be depicted in three different ways: by a set of summary propositions, by a schematic diagram, or by a tabulation of findings. I will cover each in turn. Propositions on genetic and experiential contributions to the development of aggression Aggressive social behaviours play a unique role in the biological organization and environmental adaptations of mice. The story of how aggressive acts are bound to biology and context provides an elegant illustration of how nature and nurture are interwoven over development (Cairns 1973, 1993, Cairns et a1 1990). Aggression from a developmental perspective The following generalizations have been derived from those observations: (1) Social interactions, including aggressive behaviours, play a key role in modifying the biological organization of individuals and in the structuring of their physical and social environments. Simply stated, social interactions serve two distinct functions in organismic and contextual adaptation. First, they provide for rapid and/or reversible accommodations. It would not make survival sense for individuals to fight and attack regardless of their opposition or likelihood of being injured. Accordingly, actions must be constantly coordinated with the relationship, the context, and momentary effectiveness of the behaviour.
  • Book cover image for: Origins of Aggression
    • Willard W. Hartup, Jan de Wit, Willard W. Hartup, Jan de Wit(Authors)
    • 2019(Publication Date)
    Then the means by which aggression is affected must be determined. Considering first genetic differences, these may influence aggression by diverse routes such as the production of changes in effectors or in the stimuli presented to another individual, or changes in the ability to profit by experience, or in diverse other mechanisms as well as in those specifically associated with aggression. But there is also a special difficulty in studying genetic influences on aggression in mammals which arises from the facts that (a) aggressiveness is also affected by the early social environment, and especially by the type of maternal care received; (b) the early social environment provided by the social companions is influenced by their genetic constitution, and this (especially in the case of the mother) is likely to be closely linked to that of the subject; and (c) the early social experience depends on interactive relationships, so that, for instance, the maternal care received depends on the behavior of the subject as well as on that of the mother. The possible complexities are considerable (Figure 5). Turning now to studies of the influence of experiential factors on aggression, it seems important that the factors manipulated in ex-perimental studies should be relatively small. For example, the usefulness of assessing the effects of rearing animals in isolation Figure 5. Diagrammatic representation of the complexities arising in studies of the genetic bases of aggression in mammals. The discontinuous lines indicate the effects of unspecified causal factors Genetic constitution of social companions > I Social behavior of companions Interactional T relationship N Genetic constitution of subject Social behavior of subject Aggressive behavior of subject The study of aggression 13 seems rather doubtful. Rearing in isolation is such an extreme con-dition and could affect aggression in diverse ways.
  • Book cover image for: Biosocial Theories of Crime
    • Kevin M. Beaver, KevinM. Beaver, Anthony Walsh(Authors)
    • 2017(Publication Date)
    • Routledge
      (Publisher)
    Table 1 summarizes the text. The research designs covered here are not intended to be exhaustive but are intended to illustrate what kinds of studies can be done using the logic of behavioral-genetic methods.

    Question 1: Is Children’s Aggression Wholly Accounted for by Genetic Factors, or Does It Have Nongenetic Causes as Well?

    More than 100 studies have addressed the question of genetic influence on antisocial behavior (Moffitt, in press), and metaanalyses conclude that genes influence 40% to 50% of population variation in antisocial behavior (Miles & Carey, 1997; Rhee & Waldman, 2002). This research unequivocally proves that environmental influences account for variation. This fact constitutes a remarkable contribution to the understanding of causation (Plomin, 1994). In addition, it is recognized that the heritability coefficient indexes not only the direct effects of genes but also the effects of interactions between genes and family-wide environments (Boomsma & Martin, 2002; Rutter & Silberg, 2002). In such interactions, the effect of an environmental risk may be even larger than previously reported among the subgroup of individuals having a vulnerable genotype. This is the case for antisocial behaviors.
    One useful feature of behavioral-genetic research designs is that they offer two powerful methods for documenting the importance of environmental effects (Plomin, DeFries, McClearn, & McGuffin, 2001). One of these methods of detecting environmental influence tests whether any of the family members in a study sample are more similar than can be explained by the proportion of genes they share. For instance, monozygotic (MZ) twins’ genetic similarity is twice that of dizygotic (DZ) twins and, therefore, if nothing but genes influenced antisocial behavior, MZ twins’ behavior ought to be at least twice as similar as that of DZ twins. If that is not the case, then it can be assumed that something environmental has influenced the twins and enhanced their similarity. For almost all human behavioral traits studied thus far, environmental factors shared by family members (variously labeled the “family-wide,” “common,” or “shared” environment) have not been found to make family members similar (Rowe, 1994). Antisocial behavior is a marked exception. A comparison of shared environment effects across 10 psychiatric disorders revealed that such effects were stronger for antisocial personality and conduct disorder than for affective, anxiety, or substance disorders (Ken-dler, Prescott, Myers, & Neale, 2003).
  • Book cover image for: Molecular Mechanisms Influencing Aggressive Behaviours
    • Gregory R. Bock, Jamie A. Goode, Gregory R. Bock, Jamie A. Goode(Authors)
    • 2006(Publication Date)
    • Wiley
      (Publisher)
    2005 Molecular mechanisms in£uencing aggressive behaviours. Wiley, Chichester (Novartis Foundation Symposium 268) p 227^241 A role for genetic factors in aggression? It is our common experience that there is a strong sex bias in antisocial behaviour (ASB) in humans, with males having much greater tendency towards violence than females. For example, in a longitudinal study of about 1000 individuals of both sexes from an age of three to 21, reviewed in depth by Mo⁄t et al (2001), ASB was found to be overall 2.4 times more prevalent in males than females. Evidence also points to a higher heritability of aggression in males, whereas common environment may be more important in females (Miles & Carey 1997, Vierikko et al 2003). Although there is a correlation between a rise in hormone levels and ASB in adolescent males and the relationship between testosterone and aggression has 227 been demonstrated through correlational and experimental studies in animals (Turner 1994), evidence for a direct role of testosterone in determining aggression in humans is not clear-cut (e.g. see Archer 1991, Turner 1994, van Honk et al 1999). We must therefore have an open mind concerning the possible in£uence of other genes that may contribute to a greater propensity to aggression in males. This chapter reviews our work and that of others in examining the potential role of speci¢c genetic factors, unrelated to those directly implicated in sex determination, in predisposing this sex imbalance of behavioural phenotypes. Given the observation that experience of abuse greatly increases the probability of antisocial personality and subsequent violent o¡ending in males (e.g. Rutter et al 1998), it focuses on the role of MAOA variants in ASB and the cycle of violence in maltreated males.
  • Book cover image for: Aggressive Behavior
    eBook - ePub

    Aggressive Behavior

    Genetic and Neural Approaches

    • Edward C. Simmel, Martin E. Hahn, James K. Walters, Edward C. Simmel, Martin E. Hahn, James K. Walters(Authors)
    • 2021(Publication Date)
    • Routledge
      (Publisher)
    Behavioural genetics . Amsterdam: North Holland, 1974.
  • Lagerspetz, K. M. J. , & Lagerspetz, K. Y. H. The expression of the genes of aggressiveness in mice: The effect of androgen on aggression and sexual behaviour in females. Aggressive Behav- ior , 1975, 1, 291–296.
  • Lagerspetz, K. M. J. , & Sandnabba, K. The decline of aggressiveness in male mice during group caging as determined by punishment delivered by the cage mates. Aggressive Behavior , 1982, 8, 319–334.
  • Lagerspetz, K. Y. H., Tirri, R., & Lagerspetz, K. M. J. Neurochemical and endocrinological studies of mice selectively bred for aggressiveness. Scandinavian Journal of Psychology , 1968, 9, 157–160.
  • Manning, A. Th. place of genetics in the study of behavior. In P. P. G. Bateson & R. A. Hinde (Eds.), Growing points in ethology . Cambridge, Eng.: Cambridge University Press, 1976.
  • Mather, K. Biometrical genetics: The study of continuous variation . London: Methuen, 1949.
  • Mather, K. , & Jinks, J. L. Introduction to biometrical genetics . London: Chapman and Hall, 1977.
  • Maxson, S. C. The Genetics of Aggression in vertebrates. In P. F. Brain, & D. Benton (Eds.), The biology of aggression . The Netherlands: Sijthoff/Noordhoff, 1981.
  • McClearn, G. E. , & DeFries, J. C. Introduction to behavioral genetics . San Francisco: Freeman, 1973.
  • Scott, J. P. Social genetics. Behavior Genetics , 1977, 7, 327–346.
  • Scott, J. P. The evolution of function in agonistic behavior. In P. F. Brain & D. Benton (Eds.), Multidisciplinary approaches to aggression research . Amsterdam: Elsevier/North-Holland Biomedical Press, 1981.
  • Svensson, T. W. , & Thieme, G. An investigation of a new instrument to measure motor activity of small animals. Psychopharmacologia , 1969, 14, 157–163.
  • van Abeelen, J. H. F. Genetic analysis of behavioural responses to novelty in mice. Nature , 1975, 254, 239–241.
  • van Oortmerssen, G. A. , & Bakker, T. C. M. Artificial selection for short and long attack latencies in wild Mus musculus domesticus. Behavior Genetics , 1981, 11
  • Book cover image for: The SAGE Handbook of Personality and Individual Differences
    eBook - ePub

    The SAGE Handbook of Personality and Individual Differences

    Volume III: Applications of Personality and Individual Differences

    • Virgil Zeigler-Hill, Todd K. Shackelford, Virgil Zeigler-Hill, Todd K. Shackelford, Author(Authors)
    • 2018(Publication Date)
    8 Aggression
    Wayne A. Warburton
    Craig A. Anderson
    ‘If it's natural to kill, how come men have to go into training to learn how?’ Joan Baez (1968: 136)
    Every history of humanity is peppered with incidents related to human aggression – war, conflict, interpersonal violence, and everyday hurts and harms. Although the contexts range widely, societal aggression and violence are ultimately driven by the intent of one person to hurt another, with some people being much more predisposed to aggression than others. For this reason, understanding within-person factors that increase an individual's likelihood of aggression is crucial to identifying the causes of aggressive behavior as well as the strategies that have the best chance of moderating it. This chapter examines aggressive behavior through the lens of a current model of aggression – the General Aggression Model (GAM; Anderson and Bushman, 2002; Gilbert et al., 2017; Warburton and Anderson, in press) – that emphasizes the way in which an individual's characteristics interact with situational cues and triggers from the environment to produce aggressive behavior.
    Central to the GAM is prior research about factors within a person that predispose them to aggression – individual differences in traits, genetics, biology, and learned experience that make one person more likely than another to behave aggressively. Because the GAM is a model of the processes that leads to an individual behaving aggressively in the moment, it also describes the underlying biological, neurocognitive, social, and other psychological factors and processes that may influence an episode of aggression. It also incorporates outcomes of the aggressive event, that is, the learnings that feed back into the person's stable psychological makeup, learnings that change the person's expectations and beliefs about how well or poorly future aggressive (or non-aggressive) behaviors will work. Of course, individual differences in the predisposition to aggress can never fully explain aggressive behavior. Environmental factors that trigger aggressive tendencies are also important factors in the aggression equation, and are prominent in the GAM as well.
  • Book cover image for: Control of Aggression
    eBook - ePub

    Control of Aggression

    Implications from Basic Research

    • Stanton Wheeler, John F. Knutson(Authors)
    • 2017(Publication Date)
    • Routledge
      (Publisher)
    3Genetics and Mouse Aggression G. E. Mcclearn and J. C. Defries
    Gerald McClearn completed his Ph.D. degree at the University of Wisconsin. His experience includes fellowships at the Institute of Animal Genetics in Edinburgh, Scotland and Gauthen Laboratory in London. Presently Dr. McClearn is the director of the Institute for Behavioral Genetics at the University of Colorado. His research has covered the broad spectrum of behavior genetics.
    Professor John C. DeFries received his bachelor's degree in agriculture from the University of Illinois. Subsequently, he completed both the M.A. and Ph.D. in quantitative genetics at the University of Illinois. After completing the Ph.D., he remained on the faculty of the University of Illinois until 1967, when he joined the faculty of the University of Colorado. Dr. DeFries is currently professor in the Institute of Behavioral Genetics, and a lecturer in the Department of Biology and the Department of Psychology at the University of Colorado. In addition, he has been a research fellow at the University of California, Berkeley, and visiting professor of genetics at the University of Hawaii. In 1969 Professor DeFries was invited as a visiting lecturer to the N.A.T.O. Advanced Studies Institute in Psycho genetics at the University of Birmingham, England. He is currently editor of Behavior Genetics.
    The causes of aggression are currently being examined with an unprecedented vigor, impelled by the urgency of many of our contemporary social problems, The social, behavioral, and biological sciences are all concerned with this evaluation, and the data and concepts from their respective domains are being invoked in the attempt to understand the causes of violence. Unfortunately, a residual from the old nature-nurture controversy impedes the exchange of ideas and concepts among these various disciplines. There often appears to be among social scientists an implicit (and sometimes explicit) belief that any point conceded to biological factors is one point less for social and environmental factors. This attitude reflects a dichotomous view of behavioral determination which is as unwarranted as it is widespread. There is no merit in the old proposition that pits “nature” against “nurture” as logically incompatible forces. On the contrary, genes and environmental forces interact from the moment of conception. Thus, the effects of a given genetic difference between people may be greater or less depending upon the environmental circumstances in which they reside. Similarly, the impact of an environmental agent depends upon the hereditary nature of the individual upon whom it impinges.
  • Book cover image for: Aggression
    eBook - ePub

    Aggression

    Individual Differences, Alcohol And Benzodiazepines

    • Alyson Bond, Malcolm Lader, Jose da Silveira(Authors)
    • 2013(Publication Date)
    • Psychology Press
      (Publisher)
    CHAPTER ONE

    The psychology of aggression

    In this chapter, definitions and theories of aggressive behaviour are discussed. Several factors are important in aggressive behaviour and these are discussed under three broad headings: interpersonal factors, external factors, and individual differences.

    TERMINOLOGY

    Aggression is a word that in ordinary language encompasses a wide range of behaviours. However, these sometimes diverse behaviours seem to have a common thread and the aim of a psychological definition is to explain this. There have been many definitions of aggression. For example, Harre and Lamb (1983, p.13) catalogued more than 250. These various definitions seem to share the idea that aggression involves inflicting harm or damage but beyond this, there are a number of differences. For example, does the damage have to be inflicted on a living creature or does damage to objects or property also count as aggression? Does the damage have to be physical as argued by Zillman (1978) or does psychological harm such as saying something hurtful or damaging someone's reputation also constitute an aggressive act? Given that these distinctions may be important, one solution is to define aggression broadly but then describe different types of aggression. This approach has been taken by Buss (1961) who said aggression could be physical or verbal, active or passive, direct or indirect. Combining these factors yields eight types of aggression altogether.
    Another issue, perhaps less easily resolved, concerns whether the damage or harm must be inflicted intentionally for the act to be considered aggressive. On the one hand it seems desirable to exclude inflicting harm accidentally, e.g. accidentally hitting someone with an object or saying something tactless without thinking. On the other hand, intentions cannot be observed and it may cause problems to use a definition that rests on unobservable behaviour. This was the view of Buss (1961) and Bandura (1973) whose definitions ignore the intentions that may lie behind the "response that delivers noxious stimuli to another organism". Despite these difficulties, many authors have included intention in their definitions of aggression. For example, Dollard, Doob, Miller, Mowrer, and Sears (1939) defined aggression as "an act whose goal-response is injury to an organism". Berkowitz (1974) also argues that intention is crucial. This was taken up by Geen (1976) whose working definition can be summarised in three points: (1) "Aggression consists of the delivery of noxious stimuli by one organism to another"; (2) "The stimuli are delivered by the former with the intent to harm the latter"; (3) "The one delivering the stimuli expects that the probability of the stimuli reaching the source is greater than zero". Note that this definition does not specify any particular emotional state, such as anger, or any particular attitude towards the victim, such as dislike or hostility. It does specify intention to harm but this should not be taken to exclude other intentions or motives.
  • Book cover image for: Behavioral Genetics of the Mouse: Volume 1, Genetics of Behavioral Phenotypes
    • Wim E. Crusio, Frans Sluyter, Robert T. Gerlai, Susanna Pietropaolo(Authors)
    • 2013(Publication Date)
    (eds.), Aggressive Behavior: Genetic and Neural Approaches. Lawrence Erlbaum, Hillsdale, NJ, USA, pp. 89–101. Lagerspetz, K.M.J., Tirri, R., and Lagerspetz, K.Y.H. (1968) Neurochemical and endocrinological studies in mice selectively bred for aggressiveness. Scand J Psychol 9: 157–160. Lagerspetz, K.M.J. and Wuorinen, K. (1965) A cross-fostering experiment with mice selectively bred for aggressiveness and non-aggressiveness. Rep Inst Psychol Univ Turku 17: 1–6. Lahr, G., Maxson, S.C., Mayer, A., Just, W., Pilgrim, C., and Reisert, I. (1995) Transcription of the Y chromosomal gene, Sry, in adult mouse brain. Mol Brain Res 33: 179–182. 251 Section 4: Social behavior Le Roy, I., Mortaud, S., Tordjman, S., Donsez-Darcel, E., Carlier, M., Degrelle, H., et al. (1999) Genetic correlation between steroid sulfatase concentration and initiation of attack behavior in mice. Behav Genet 29: 131–136. Maxson, S.C. (1992) Methodological issues in genetic analyses of an agonistic behavior (offense) in male mice. In Goldowitz, D., Wahlsten, D., and Wimer, R. (eds.), Techniques for the Genetic Analysis of Brain and Behavior: Focus on the Mouse, Techniques in the Behavioral and Neural Sciences, Vol. 8. Elsevier, Amsterdam, pp. 349–373. Maxson, S.C. (1996) Searching for candidate genes with effects on an agonistic behavior, offense, in mice. Behav Genet 26: 471–476. Maxson, S.C. (2009) The genetics of offensive aggression in mice. In Kim, Y-K. (ed.), Handbook of Behavior Genetics. Springer, New York, pp. 301–316. Maxson, S.C. and Canastar, A. (2007) The Genetics of Aggression in mice. In Flannery, D.J., Vazony, A.T., and Waldman, I.D. (eds.), The Cambridge Handbook of Violent Behavior and Aggression. Cambridge University Press, New York, pp. 91–110. Mayer, A., Mosler, G., Just, W., Pilgrim, C., and Reisert, I. (2000) Developmental profile of Sry transcripts in mouse brain. Neurogenetics 3: 25–30. McClearn, G.E. and DeFries, J.C.
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