Changing the means of managerial work: effects of automated decision support systems on personnel selection tasks

To enhance the quality and efficiency of information processing and decision-making, automation based on artificial intelligence and machine learning has increasingly been used to support managerial tasks and duties. In contrast to classical applications of automation (e.g., within production or aviation), little is known about how the implementation of automation for management changes managerial work. In a work design frame, this study investigates how different versions of automated decision support systems for personnel selection as a specific management task affect decision task performance, time to reach a decision, reactions to the task (e.g., enjoyment), and self-efficacy in personnel selection. In a laboratory experiment, participants (N = 122) were randomly assigned to three groups and performed five rounds of a personnel selection task. The first group received a ranking of the applicants by an automated support system before participants processed applicant information (support-beforeprocessing group), the second group received a ranking after they processed applicant information (support-after-processing group), and the third group received no ranking (no-support group). Results showed that satisfaction with the decision was higher for the support-after-processing group. Furthermore, participants in this group showed a steeper increase in self-efficacy in personnel selection compared to the other groups. This study combines human factors, management, and industrial/ organizational psychology literature and goes beyond discussions concerning effectiveness and efficiency in the emerging area of automation in management in an attempt to stimulate research on potential effects of automation on managers’ job satisfaction and well-being at work

Transformations agricoles et agroalimentaires

À l’heure des robots et du numérique, la terre (habitat, agriculture, paysage, planète) et la nourriture (du corps et de l’âme) sont parmi les préoccupations majeures dans les espaces médiatiques et politiques. Le pétrole et l’abondance qui l’a accompagné nous avaient fait oublier qu’elles sont au fondement des sociétés humaines. La « crise alimentaire » de 2008, qui a secoué plusieurs continents, a rappelé aux gouvernements l’enjeu de la sécurité alimentaire. Après des décennies d’excédents, de baisse du prix des produits agricoles de base, la question de la valeur de la terre et de l’agriculture est de retour. La question de la santé et celle des droits humains prennent une place élargie tant dans les politiques publiques et dans la production de normes alimentaires. Des mouvements sociaux transnationaux s’emparent de la question de l’avenir de l’agriculture et de l’alimentation, et de celle de la « bonne vie ». Pour contribuer à cette réflexion sur l’avenir de la terre et de la nourriture, cet ouvrage étudie la socialisation de l’agriculture, c’est-à-dire sa prise en charge tant par les politiques agricoles (essentiellement nationales) que par l’organisation des marchés dans un cadre national et international. Il le fait en prenant un large recul et mobilise trois temporalités. La première est celle de la planète. La seconde, celle des régimes métaboliques, façons dont l’humanité à différents stades de développement, mobilise matériaux et énergie. La troisième est celle du capitalisme, avec la succession de systèmes hégémoniques (ce qui n’exclue pas de multiples polarités). Cet ouvrage réunit des recherches récentes d’économistes, de sociologues, d’historiens et d’agronomes, de différents pays, recherches qui ont en commun de concerner la place de l’agriculture dans l’évolution des capitalismes

Heterogeneity of Microglial Activation in the Innate Immune Response in the Brain

The immune response in the brain has been widely investigated and while many studies have focused on the proinflammatory cytotoxic response, the brain’s innate immune system demonstrates significant heterogeneity. Microglia, like other tissue macrophages, participate in repair and resolution processes after infection or injury to restore normal tissue homeostasis. This review examines the mechanisms that lead to reduction of self-toxicity and to repair and restructuring of the damaged extracellular matrix in the brain. Part of the resolution process involves switching macrophage functional activation to include reduction of proinflammatory mediators, increased production and release of anti-inflammatory cytokines, and production of cytoactive factors involved in repair and reconstruction of the damaged brain. Two partially overlapping and complimentary functional macrophage states have been identified and are called alternative activation and acquired deactivation. The immunosuppressive and repair processes of each of these states and how alternative activation and acquired deactivation participate in chronic neuroinflammation in the brain are discussed

SNAIL1-mediated downregulation of FOXA proteins facilitates the inactivation of transcriptional enhancer elements at key epithelial genes in colorectal cancer cells

<div><p>Phenotypic conversion of tumor cells through epithelial-mesenchymal transition (EMT) requires massive gene expression changes. How these are brought about is not clear. Here we examined the impact of the EMT master regulator SNAIL1 on the FOXA family of transcription factors which are distinguished by their particular competence to induce chromatin reorganization for the activation of transcriptional enhancer elements. We show that the expression of <i>SNAIL1</i> and <i>FOXA</i> genes is anticorrelated in transcriptomes of colorectal tumors and cell lines. In cellular EMT models, ectopically expressed Snail1 directly represses FOXA1 and triggers downregulation of all FOXA family members, suggesting that loss of FOXA expression promotes EMT. Indeed, cells with CRISPR/Cas9-induced FOXA-deficiency acquire mesenchymal characteristics. Furthermore, ChIP-seq data analysis of FOXA chromosomal distribution in relation to chromatin structural features which characterize distinct states of transcriptional activity, revealed preferential localization of FOXA factors to transcriptional enhancers at signature genes that distinguish epithelial from mesenchymal colon tumors. To validate the significance of this association, we investigated the impact of FOXA factors on structure and function of enhancers at the <i>CDH1</i>, <i>CDX2</i> and <i>EPHB3</i> genes. FOXA-deficiency and expression of dominant negative FOXA2 led to chromatin condensation at these enhancer elements. Site-directed mutagenesis of FOXA binding sites in reporter gene constructs and by genome-editing <i>in situ</i> impaired enhancer activity and completely abolished the active chromatin state of the <i>EPHB3</i> enhancer. Conversely, expression of FOXA factors in cells with inactive <i>CDX2</i> and <i>EPHB3</i> enhancers led to chromatin opening and <i>de novo</i> deposition of the H3K4me1 and H3K27ac marks. These findings establish the pioneer function of FOXA factors at enhancer regions of epithelial genes and demonstrate their essential role in maintaining enhancer structure and function. Thus, by repressing FOXA family members, SNAIL1 targets transcription factors at strategically important positions in gene-regulatory hierarchies, which may facilitate transcriptional reprogramming during EMT.</p></div

FOXA1 and FOXA2 bind preferentially to intergenic enhancer regions of epithelial genes.

<p>(A) Venn diagrams showing numbers of common and cell-type-specific ChIP-seq peaks of FOXA1 (left) and FOXA2 (right) in A549, HepG2, T47D and Caco2 cells. (B) Feature distribution of FOXA1 (left) and FOXA2 (right) ChIP-seq peaks for all genes (All genes) and genes differentially expressed in epithelial (Epithelial genes) or mesenchymal colon tumors (Mesench. genes). Peak locations were categorized into seven features according to their locations within 5’-UTR, 3’-UTR, promoter, exonic, downstream, intronic, or distal intergenic regions. Promoter regions were defined as 3 kb upstream and downstream of a transcription start site. Significant differences in the fractions of ChIP-seq peaks located in distal intergenic and intronic features for epithelial versus mesenchymal genes were assessed using a hypergeometric test relative to all genes. See <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1007109#pgen.1007109.s007" target="_blank">S7 Fig</a>, panel A for peak numbers. p-Values for FOXA1 occupancy at downstream regions of epithelial genes: A549: 1.076 x 10⁻⁰³ (**); HepG2: 3.451 x 10⁻⁰² (*); T47D: 0.017 (*). p-Values for FOXA2 occupancy at downstream regions of epithelial genes: A549: 1.932 x 10⁻⁰³ (**); Caco2: 0.044 (*); HepG2: 5.634 x 10⁻⁰² (*). (C) Relative (rel.) abundance of chromatin states for FOXA1 and FOXA2 ChIP-seq peak regions in distal intergenic regions of epithelial and mesenchymal genes for A549 and HepG2 cells. Genomic locations were annotated according to HMM on chromatin states. Bars denote the relative abundance of ChIP-seq peaks (in %) for 13 out of 15 states represented in the peak regions. The potential functional impact of transcription factor binding decreases from left to right: binding to an active transcription start site (TSS) to binding in a quiescent region. The numbers inside the bar plots indicate the total number of peaks for each condition.</p

FOXA1 and FOXA3 are regulators of the <i>CDH1</i>, <i>CDX2</i> and <i>EPHB3</i> enhancers.

<p>(A, C, E) Schemes of the <i>CDH1</i> (A), the <i>CDX2</i> (C), and the <i>EPHB3</i> (E) gene loci. Gene annotation is based on the Ensembl genome browser. Exons are depicted in green. Transcriptional start sites are indicated by arrows. The positions of ECRs with predicted FOX binding motifs and signals from FOXA1 ChIP-seq analyses from the ENCODE project are shown below the schemes of the gene loci. The PCR-amplified regions analyzed in ChIP experiments are indicated by black bars. (B, D, F) ChIP analyses to test for binding of FOXA1 and FOXA3 at the <i>CDH1</i> (B), the <i>CDX2</i> (D) and the <i>EPHB3</i> (F) loci in the indicated CRC cell lines. Data were calculated as percent input. Shown are the mean and SEM; n≥3. Statistical significance was calculated relative to the control regions at the respective gene loci.</p

Interfering with FOXA function alters chromatin structure at the <i>CDH1</i>, <i>CDX2</i>, and <i>EPHB3</i> enhancers.

<p>(A) FAIRE analyses of the <i>CDH1</i> +7.8 kb, the <i>CDX2</i> +10.0 kb and the <i>EPHB3</i> −2.3 kb enhancers in parental LS174T cells, the FOXA1^KOA2A3^neg cell clone 2F8, and the FOXA1^WT cell clone 1C6. As control (ctrl) the <i>AXIN2</i> locus at -11.0 kb was analyzed. Data are given as relative (rel.) FAIRE enrichment; n = 4. (B) qRT-PCR analyses to assess <i>CDH1</i>, <i>CDX2</i> and <i>EPHB3</i> relative expression (rel. expr.) levels in parental LS174T cells, FOXA1^KOA2A3^neg cell clones (1C2, 2F8), and FOXA1^WT cell clones (1C6, 1E10) as indicated. For <i>CDH1</i>, the results shown here were extracted from the data set presented in <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1007109#pgen.1007109.s005" target="_blank">S5 Fig</a>. Data are shown as mean and SEM; n = 3. (C) Assessment of E-CADHERIN (E-CAD), CDX2 and EPHB3 protein levels by Western Blotting in cytoplasmic (E-CAD, EPHB3, GSK3β) and nuclear fractions (CDX2, RNAPII) derived from parental LS174T cells, FOXA1^KOA2A3^neg cell clones (1C2, 2F8), and FOXA1^WT cell clones (1C6, 1E10). GSK3β and RNA polymerase II (RNAPII) immunodetections served as loading controls. M_W = molecular weight in kDa. (D) FAIRE analyses of the <i>CDH1</i> +7.8 kb, the <i>CDX2</i> +10.0 kb and the <i>EPHB3</i> −2.3 kb enhancers in LS174T cells stably transduced with Dox-inducible retroviral control or dnFOXA2-HA expression vectors treated without or with Dox for 96h. As control (ctrl) the <i>EPHB3</i> locus at -7.0 kb was analyzed. Data are given as relative (rel.) FAIRE enrichment; n = 4. (E) qRT-PCR analyses to assess <i>dnFOXA2-HA</i>, <i>CDH1</i>, <i>CDX2</i>, and <i>EPHB3</i> relative expression (rel. expr.) levels in LS174T cells stably transduced with Dox-inducible retroviral control or dnFOXA2-HA expression vectors. Data are shown as mean and SEM; n = 4. For detection of dnFOXA2-HA expression a primer pair amplifying cDNA from endogenous full-length FOXA2 as well as truncated dnFOXA2-HA transcripts was used. (F) Western Blot analyses showing equal E-CADHERIN (E-CAD) levels and reduced CDX2 and EPHB3 protein expression upon Dox-induced dnFOXA2-HA expression in LS174T cells stably transduced with Dox-inducible retroviral control or dnFOXA2-HA expression vectors. M_W = molecular weight in kDa. α-TUBULIN (α-TUB) immunodetection served as loading control.</p

Expression of FOXA1 or FOXA3 in HCT116 cell clones leads to chromatin opening at the <i>CDH1</i>, <i>CDX2</i> and <i>EPHB3</i> enhancers and induces changes in H3K27ac/H3K4me1 deposition.

<p>(A) FAIRE analyses showing chromatin decompaction at the <i>CDH1</i>, <i>CDX2</i>, and <i>EPHB3</i> enhancers upon Dox-induced FOXA1-HA or FOXA3-HA expression in HCT116 cells. Data are given as relative (rel.) FAIRE enrichment; n = 3. As control (ctrl) the <i>EPHB3</i> locus at -7.0 kb was analyzed. (B) ChIP analyses to test for recruitment of FOXA1-HA/FOXA3-HA to the <i>CDH1</i>, the <i>CDX2</i>, and the <i>EPHB3</i> enhancers and presence of the histone modifications H3K27ac and H3K4me1 in HCT116 cells stably transduced with Dox-inducible retroviral control, FOXA1-HA or FOXA3-HA expression vectors. Data are given as percent input (HA) or as percent input normalized (norm.) to H3 (H3K27ac, H3K4me1) to compensate for variations in nucleosome density; n = 3. As control (ctrl) the <i>EPHB3</i> locus at -10.0 kb was analyzed.</p

Mutation of the FOX binding sites at the <i>EPHB3</i> enhancer leads to chromatin compaction at the enhancer and promoter and abolishes <i>EPHB3</i> expression.

<p>(A) ChIP analysis to monitor FOXA1 occupancy at the <i>EPHB3</i> locus in LS174T cell clones genome-edited with the CRISPR/Cas9 system. Data are given as percent input. Shown is the mean and SEM; n≥3. Statistical significance was calculated relative to the LS174T wild-type cell pool. (B) FAIRE analyses to test chromatin compaction at the <i>EPHB3</i> enhancer and promoter in LS174T cell clones genome-edited with the CRISPR/Cas9 system. Data are given as relative (rel.) FAIRE enrichment; n = 3. Statistical significance was calculated relative to the LS174T wild-type cell pool. (C) ChIP analyses to monitor presence of the histone modifications H3K27ac and H3K4me1 at the <i>EPHB3</i> locus in LS174T cell clones genome-edited with the CRISPR/Cas9 system. Data are given as percent input normalized (norm.) to H3 to compensate for variations in nucleosome density; n≥3. Statistical significance was calculated relative to the LS174T wild-type cell pool. (D) qRT-PCR (upper) and Western Blot (lower) analyses to assess EPHB3 expression in LS174T cell clones with mutations in transcription factor binding sites at the <i>EPHB3</i> enhancer. Data are shown as mean and SEM; n = 3; rel. expr.: relative expression. M_W = molecular weight in kDa. α-TUBULIN (α-TUB) immunodetection served as loading control.</p