A typology of user liability to IT addiction Vaghefi, Isaac; Lapointe, Liette; Boudreau‐Pinsonneault, Camille
Information systems journal (Oxford, England),
March 2017, Volume:
27, Issue:
2
Journal Article
Peer reviewed
To date, information systems (IS) research mainly has provided a monolithic view of information technology (IT) use, considering it to be a desired behaviour with positive outcomes. However, given ...the dramatic increase in the use of technology during the last few years, susceptibility to IT addiction is increasingly becoming an important issue for technology users and IS researchers. In this paper, we report the results of a study that focuses on identifying variations in user liability to IT addiction, which reflects the susceptibility of individual users to develop IT addiction. First, a review of the literature in different disciplines (e.g. health, psychology and IS) allows us to better understand the concepts of IT addiction and liability to addiction. The literature review also provides an overview of the antecedents and consequences associated with IT addiction. Then, building on the analysis of 15 in‐depth interviews and 182 exploratory open‐ended surveys collected from smartphone users, we apply the concept of liability to addiction in the IT use context and propose a typological theory of user liability to IT addiction. Our typology reveals five ideal types; each can be associated to a user profile (addict, fanatic, highly engaged, regular and thoughtful). Building upon both the extant literature and our results, we put forth propositions to extend the theoretical contributions of the study. We finally discuss the contributions and implications of our paper for research and practice.
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BFBNIB, FZAB, GIS, IJS, IZUM, KILJ, NLZOH, NUK, OILJ, PILJ, SAZU, SBCE, SBMB, UL, UM, UPUK
The balance of contralateral and ipsilateral retinogeniculate projections is critical for binocular vision, but the transcriptional programs regulating this process remain ill defined. Here we show ...that the Pou class homeobox protein POU3F1 is expressed in nascent mouse contralateral retinal ganglion cells (cRGCs) but not ipsilateral RGCs (iRGCs). Upon Pou3f1 inactivation, the proportion of cRGCs is reduced in favor of iRGCs, leading to abnormal projection ratios at the optic chiasm. Conversely, misexpression of Pou3f1 in progenitors increases the production of cRGCs. Using CUT&RUN and RNA sequencing in gain- and loss-of-function assays, we demonstrate that POU3F1 regulates expression of several key members of the cRGC gene regulatory network. Finally, we report that POU3F1 is sufficient to induce RGC-like cell production, even in late-stage retinal progenitors of Atoh7 knockout mice. This work uncovers POU3F1 as a regulator of the cRGC transcriptional program, opening possibilities for optic nerve regenerative therapies.
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•POU3F1 is expressed in postmitotic RGC precursors but downregulated in most mature RGCs•Pou3f1 loss increases production of ipsilateral RGCs at the expense of contralateral RGCs•POU3F1 represses ipsilateral determinants and activates contralateral determinants•POU3F1 promotes RGC-like cell production when misexpressed in late progenitors
Fries et al. demonstrate that POU3F1 is expressed in postmitotic retinal ganglion cell (RGC) precursors, where it represses Atoh7 and the ipsilateral determinant Zic2, while promoting expression of several contralateral determinants, leading to the generation of contralateral RGCs. This work uncovers a developmental regulator of cells involved in binocular vision.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
4.
Cell reprogramming: Nature does it too Boudreau-Pinsonneault, Camille; Cayouette, Michel
CB/Current biology,
11/2021, Volume:
31, Issue:
21
Journal Article
Peer reviewed
Open access
Cell reprogramming is generally considered an artificially induced event. Excitingly, a new study shows that post-mitotic cell reprogramming occurs naturally in the developing fish retina, uncovering ...a mechanism involved in the generation of cell diversity.
Cell reprogramming is generally considered an artificially induced event. Excitingly, a new study shows that post-mitotic cell reprogramming occurs naturally in the developing fish retina, uncovering a mechanism involved in the generation of cell diversity.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Heterozygous loss-of-function mutations in GRIN2B, a subunit of the NMDA receptor, cause intellectual disability and language impairment. We developed clonal models of GRIN2B deletion and ...loss-of-function mutations in a region coding for the glutamate binding domain in human cells and generated neurons from a patient harboring a missense mutation in the same domain. Transcriptome analysis revealed extensive increases in genes associated with cell proliferation and decreases in genes associated with neuron differentiation, a result supported by extensive protein analyses. Using electrophysiology and calcium imaging, we demonstrate that NMDA receptors are present on neural progenitor cells and that human mutations in GRIN2B can impair calcium influx and membrane depolarization even in a presumed undifferentiated cell state, highlighting an important role for non-synaptic NMDA receptors. It may be this function, in part, which underlies the neurological disease observed in patients with GRIN2B mutations.
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•Non-synaptic NMDA receptors are crucial for development of forebrain neural stem cells•Mutations in GRIN2B impair neuronal differentiation•Engineered patient repair restores cell differentiation•Pharmacological blockade of NMDA receptors impairs differentiation
Mutations in GRIN2B cause intellectual disability and language impairments. In this study, Bell and colleagues engineer mutations in GRIN2B and repair a patient missense mutation to show an important role for GRIN2B and non-synaptic NMDA receptors in differentiating neural stem cells.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Direct neuronal reprogramming by temporal identity factors Boudreau-Pinsonneault, Camille; David, Luke Ajay; Lourenço Fernandes, José Alex ...
Proceedings of the National Academy of Sciences - PNAS,
05/2023, Volume:
120, Issue:
19
Journal Article
Peer reviewed
Open access
Temporal identity factors are sufficient to reprogram developmental competence of neural progenitors and shift cell fate output, but whether they can also reprogram the identity of terminally ...differentiated cells is unknown. To address this question, we designed a conditional gene expression system that allows rapid screening of potential reprogramming factors in mouse retinal glial cells combined with genetic lineage tracing. Using this assay, we found that coexpression of the early temporal identity transcription factors Ikzf1 and Ikzf4 is sufficient to directly convert Müller glial (MG) cells into cells that translocate to the outer nuclear layer (ONL), where photoreceptor cells normally reside. We name these "induced ONL (iONL)" cells. Using genetic lineage tracing, histological, immunohistochemical, and single-cell transcriptome and multiome analyses, we show that expression of Ikzf1/4 in MG in vivo, without retinal injury, mostly generates iONL cells that share molecular characteristics with bipolar cells, although a fraction of them stain for Rxrg, a cone photoreceptor marker. Furthermore, we show that coexpression of Ikzf1 and Ikzf4 can reprogram mouse embryonic fibroblasts to induced neurons in culture by rapidly remodeling chromatin and activating a neuronal gene expression program. This work uncovers general neuronal reprogramming properties for temporal identity factors in terminally differentiated cells.
Cell division orientation is crucial to control segregation of polarized fate determinants in the daughter cells to produce symmetric or asymmetric fate outcomes. Most studies in vertebrates have ...focused on the role of mitotic spindle orientation in proliferative asymmetric divisions and it remains unclear whether altering spindle orientation is required for the production of asymmetric fates in differentiative terminal divisions. Here, we show that the GoLoco motif protein LGN, which interacts with Gαi to control apicobasal division orientation in Drosophila neuroblasts, is excluded from the apical domain of retinal progenitors undergoing planar divisions, but not in those undergoing apicobasal divisions. Inactivation of LGN reduces the number of apicobasal divisions in mouse retinal progenitors, whereas it conversely increases these divisions in cortical progenitors. Although LGN inactivation increases the number of progenitors outside the ventricular zone in the developing neocortex, it has no effect on the position or number of progenitors in the retina. Retinal progenitor cell lineage analysis in LGN mutant mice, however, shows an increase in symmetric terminal divisions producing two photoreceptors, at the expense of asymmetric terminal divisions producing a photoreceptor and a bipolar or amacrine cell. Similarly, inactivating Gαi decreases asymmetric terminal divisions, suggesting that LGN function with Gαi to control division orientation in retinal progenitors. Together, these results show a context-dependent function for LGN and indicate that apicobasal divisions are not involved in proliferative asymmetric divisions in the mouse retina, but are instead essential to generate binary fates at terminal divisions.
The mammalian central nervous system (CNS) is mostly devoid of regenerative abilities. Injuries and degenerative disorders hence lead to irreversible loss of neurons and can result in devastating ...impairments. Stimulating endogenous regeneration, as occurs in lower vertebrates, would allow mammals to restore tissue integrity and function. Glia have been identified as a potential source of regeneration in the CNS since they are present in large numbers, are resistant to trauma, and some have the capacity to proliferate. Here, we take advantage of the retina as a model system to investigate glia-mediated CNS endogenous regeneration. We initially examine the regenerative potential of the main retinal glia, Müller glia, after injury and growth factor treatments. We find that these manipulations are not sufficient to induce robust regenerative capacities in Müller glia, sparking the need for novel methods to achieve this. We follow up by investigating whether temporal identity factors, which instruct, and can reprogram, the temporal competence of neural progenitors during development, could similarly reprogram the identity of differentiated cells. We find that co-expression of the temporal identity factor Ikzf1, with its family member Ikzf4, is sufficient to convert adult mouse retinal glia into neuron-like cells with mixed cone and bipolar identities. We also report that co-expression of Ikzf1 and Ikzf4, along with Brn2 and Myt1l, are sufficient to reprogram mouse embryonic fibroblasts into induced neurons by quickly increasing chromatin accessibility of neuronal-specific genes and inducing their expression. Work presented in this thesis identifies novel neuronal reprogramming factors, and uncovers new therapeutic opportunities for neurodegeneration
Defined as the dependency to a technology that results in its excessive and compulsive use, IT addiction is seen as increasingly prevalent in today's societies. Recent research has revealed that IT ...addictive behaviors are creating serious problems for individuals and organizations alike. In this paper, we report the results of a qualitative study that aimed at investigating smart phone addictive usage. Building on 11 in-depth interviews and answers to 183 exploratory written questionnaires, we used a grounded theory approach to investigate this phenomenon. Our results reveal four smarphone user profiles. In two of these profiles, users are exhibiting addictive behaviors. In the first group, the users' profile corresponds to that of other types of additions. In the second group, known definitions of addiction do not apply and the characteristics of these users are very different. Our results thus suggest that adopting traditional conceptualizations of addiction will not be sufficient to define, understand and manage IT addictive behaviors.
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