INVISIBLE LABOR FOR DATA: INSTITUTIONS, INFRASTRUCTURE, AND VIRTUAL SPACE

Americans are accustomed to a wide range of data collection in their lives: census, polls, surveys, user registrations, and disclosure forms. When logging onto the Internet, users’ actions are being tracked everywhere: clicking, typing, tapping, swiping, searching, and placing orders. All of this data is stored to create data-driven profiles of each user. Social network sites, furthermore, set the voluntarily sharing of personal data as the default mode of engagement. But people’s time and energy devoted to creating this massive amount of data, on paper and online, are taken for granted. Few people would consider their time and energy spent on data production as labor. Even if some people do acknowledge their labor for data, they believe it is accessory to the activities at hand. In the face of pervasive data collection and the rising time spent on screens, why do people keep ignoring their labor for data? How has labor for data been become invisible, as something that is disregarded by many users? What does invisible labor for data imply for everyday cultural practices in the United States? Invisible Labor for Data addresses these questions. I argue that three intertwined forces contribute to framing data production as being void of labor: data production institutions throughout history, the Internet’s technological infrastructure (especially with the implementation of algorithms), and the multiplication of virtual spaces. There is a common tendency in the framework of human interactions with computers to deprive data and bodies of their materiality. My Introduction and Chapter 1 offer theoretical interventions by reinstating embodied materiality and redefining labor for data as an ongoing process. The middle Chapters present case studies explaining how labor for data is pushed to the margin of the narratives about data production. I focus on a nationwide debate in the 1960s on whether the U.S. should build a databank, contemporary Big Data practices in the data broker and the Internet industries, and the group of people who are hired to produce data for other people’s avatars in the virtual games. I conclude with a discussion on how the new development of crowdsourcing projects may usher in the new chapter in exploiting invisible and discounted labor for data.

Genome Wide Association Studies of Phagocytosis and the Cellular Immune Response in Drosophila melanogaster.

Phagocytosis of bacteria by specialized blood cells, known as hemocytes, is a vital component of Drosophila cellular immunity. To identify novel genes that mediate the cellular response to bacteria, we conducted three separate genetic screens using the Drosophila Genetic Reference Panel (DGRP). Adult DGRP lines were tested for the ability of their hemocytes to phagocytose the Gram-positive bacteria Staphylococcus aureus or the Gram-negative bacteria Escherichia coli. The DGRP lines were also screened for the ability of their hemocytes to clear S. aureus infection through the process of phagosome maturation. Genome-wide association analyses were performed to identify potentially relevant single nucleotide polymorphisms (SNPs) associated with the cellular immune phenotypes. The S. aureus phagosome maturation screen identified SNPs near or in 528 candidate genes, many of which have no known role in immunity. Three genes, dpr10, fred, and CG42673, were identified whose loss-of-function in blood cells significantly impaired the innate immune response to S. aureus. The DGRP S. aureus screens identified variants in the gene, Ataxin 2 Binding Protein-1 (A2bp1) as important for the cellular immune response to S. aureus. A2bp1 belongs to the highly conserved Fox-1 family of RNA-binding proteins. Genetic studies revealed that A2bp1 transcript levels must be tightly controlled for hemocytes to successfully phagocytose S. aureus. The transcriptome of infected and uninfected hemocytes from wild type and A2bp1 mutant flies was analyzed and it was found that A2bp1 negatively regulates the expression of the Immunoglobulin-superfamily member Down syndrome adhesion molecule 4 (Dscam4). Silencing of A2bp1 and Dscam4 in hemocytes rescues the fly’s immune response to S. aureus indicating that Dscam4 negatively regulates S. aureus phagocytosis. Overall, we present an examination of the cellular immune response to bacteria with the aim of identifying and characterizing roles for novel mediators of innate immunity in Drosophila. By screening panel of lines in which all genetic variants are known, we successfully identified a large set of candidate genes that could provide a basis for future studies of Drosophila cellular immunity. Finally, we describe a novel, immune-specific role for the highly conserved Fox-1 family member, A2bp1.