Genetic engineering promises human control over life itself but relies on techno-scientific mysticism to blur its challenges. I explore some of the biopolitics of genetic engineering in chapter four of my 2008/2011 book, Governmentality, Biopower, and Everyday Life.
Genetic engineering was based on a molecular view of life that sought to understand and govern life at its most basic levels. Genetic engineering is atomistic and mechanistic in its formulation of life, premised on the mistaken idea that each gene expresses only a single type of protein. Genetic engineering was constituted within a military-industrial nexus and has created new forms of biocapital.
We see how genetic engineering operates as biocapital in the patent battle over the crispr gene editing technology being waged between: 1) Univ. of California Berkeley and Univ of Vienna and 2) Broad Institute Partnership between Harvard and MIT:
Joe Palazzolo and Amy Dockser Marcus. (2016, December 6). Who Owns Key Gene Technology? Question Heads to Court. The Wall Street Journal, http://www.wsj.com/articles/rival-research-teams-head-to-court-1480939203
Gene-editing tool Crispr-Cas9 has spurred millions in investments; rival research teams claim patents.... A panel of patent judges in Alexandria, Va., is slated to hear arguments from lawyers for both sides on Tuesday in what amounts to the close of the dispute’s first act. The Patent Trial and Appeal Board must decide whether the parties’ claims add up to inventions that are truly in conflict. In the second and final act, likely to unfold next year, the panel will determine which side owns the commercial rights to Crispr.
The Crispr-Cas9 gene editing tool has promised to deliver precision engineering that allegedly will achieve human control over biological life. The realities are of course much more complicated.
Here is an excerpt from my Governmentality, Biopower and Everyday Life book about the role of epigenetics and other systemic influences in shaping gene expression:
Research on epigenetic change has profound implications for taken-for-granted assumptions about the relationship between the genotype and phenotype, and points to the limited value of sequencing data to conclusively predict disease or disease expression.
Epigenetics involves regulation of gene expressions, entailing:the regulation of changes in gene expression by mechanisms that do not involve changes in DNA sequence. Epigenetic changes encompass chromatic structure modulation, transcriptional repression, X-chromosome inactivation, genomic imprinting, and the suppression of the detrimental effects of repetitive and parasitic DNA sequences on genome integrity. (National Cancer Institute, 2006)
Epigenetics explain why identical twins afflicted with cystic fibrosis might have significant divergences in the expressions of their disease. Accordingly, Reiner Veitia (2005) suggested the very idea of a clone needs to be rethought as a consequence of the degree of phenotypic variation expressed in an organism not encoded in its genome. Conceptualizations of clones (based on sequenced comparisons) involve a “statistical over-simplification representing a series of individuals having essentially the same genome but capable of exhibiting wide phenotypic variation” (p. 21).
Complementing the study of epigenetic processes is proteomics, the examination of how proteins are expressed under different biochemical conditions. Proteomics studies post-translational modification to proteins, and therefore extends beyond analysis of epigenetic regulation of gene expression (Strohman, 2002). Other areas of research, including study of networks of glycolysis and mitochondrial oxidation-reduction, require research to address dynamic systems of interaction across molecular environments.
Taken together, epigenetics, proteomics, and the study of metabolic networks (e.g., metabolomics) de-couple mechanistic linear formulations of the genotype-phenotype relationship and demonstrate the limits of sequencing data’s capacities to reveal the dynamics of living bodies.
The emerging “dynamic” sciences linking DNA sequences with translation and post-translation processes again implicate environmental threats. For example, although some epigenetic factors may be internal (endogenous) to the organism, many are not. As the article from the National Cancer Institute (2006) explains, “A variety of chemicals, certain base analogs, radiation, smoke, stress, hormones [such as estradiol], butyryl cAMP, bromobenzene, other agents [such as nickel, arsenic, cadmium], and reactive oxygen species can alter the phenotypes of mammalian cells epigenetically.”
The most commonly observed epigenetic change occurs when chemical groups attach to DNA, resulting in silencing of a nearby gene (Winstead, 2005). Research suggests dietary alterations can produce changes in DNA methylation, which can impact the phenotype (Waterland & Jirtle, 2003). It is believed epigenetic changes play a role in cancer development, particularly when they affect genes that suppress tumors and/or regulate growth.
By stressing factors regulating gene expression, and the production and regulation of proteins, new research has the potential effect of expanding the perception and calculation of risk to encompass environmental forces. The study of dynamic biological processes also offers opportunities for interventions designed to regulate gene expression, protein production, and metabolic processes. For example, researchers suggest targeting unwanted epigenetic changes (e.g., methylation) may be far easier in the long run than reversing genetic mutations (Winstead, 2005).
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