Migration as hope and depression: existential im/mobilities in and beyond Egypt

Recent scholarship has asserted that prolonged periods of‘waiting’or‘stuckedness’are becoming the condition of modern capitalism for manypeople. This article complicates this assertion by interrogating the affectivelife of migration, an act which offers the possibility of overcoming, but alsoreinforces, existential stuckedness. Using two ethnographies with youngaspiring male migrants in Egypt, and older migrant men in the Netherlands,we reveal how migration, both before and after physical movement, isexperienced through constant existential oscillation: between‘‘amal’(hope) that the good life is arriving, and‘ikti’āb’(anEgyptianunderstandingof depression) when a new blockage is met. Developing existing under-standings of migratory experience and governance, the article argues thatoscillation emerges out of‘cruel’migratory regimes which perpetually offerup the promise of the good life to aspiring migrants, while inhibiting themeans of achieving it for the majority Horizon 2020(H2020)640074FSW - Global Connections --- OudGlobal Challenges (FSW

Welfare, social citizenship, and the spectre of inequality in Amsterdam

This article explores how notions of citizenship are negotiated in encounters between parents and youth care professionals in Amsterdam in the context of heated debates over citizenship and belonging. We draw on ethnographic research on Egyptian migrant parents' interactions with the welfare state, and on the work of youth care professionals. We found that both parents and professionals were invested in universal forms of citizenship. Parents wanted to be treated like their fellow citizens regardless of their background, while professionals wanted to care for all children. While parents feared and suspected that their children were subject to unfair treatment, professional practices left little space for disagreement or a consideration of racialized aspects of their encounters with clients. We conclude that notions of equal citizenship provide a primary, but uncertain ground for the elaboration of citizenship and belonging in parenting encounters, which is haunted by the spectre of difference and inequality.Horizon 2020(H2020)Global Challenges (FSW

Reproducing Europe: migrant families, professionals and the welfare state

Horizon 2020(H2020)640074Global Challenges (FSW

Caenorhabditis elegans Cyclin D/CDK4 and Cyclin E/CDK2 Induce Distinct Cell Cycle Re-Entry Programs in Differentiated Muscle Cells

Cell proliferation and differentiation are regulated in a highly coordinated and inverse manner during development and tissue homeostasis. Terminal differentiation usually coincides with cell cycle exit and is thought to engage stable transcriptional repression of cell cycle genes. Here, we examine the robustness of the post-mitotic state, using Caenorhabditis elegans muscle cells as a model. We found that expression of a G1 Cyclin and CDK initiates cell cycle re-entry in muscle cells without interfering with the differentiated state. Cyclin D/CDK4 (CYD-1/CDK-4) expression was sufficient to induce DNA synthesis in muscle cells, in contrast to Cyclin E/CDK2 (CYE-1/CDK-2), which triggered mitotic events. Tissue-specific gene-expression profiling and single molecule FISH experiments revealed that Cyclin D and E kinases activate an extensive and overlapping set of cell cycle genes in muscle, yet failed to induce some key activators of G1/S progression. Surprisingly, CYD-1/CDK-4 also induced an additional set of genes primarily associated with growth and metabolism, which were not activated by CYE-1/CDK-2. Moreover, CYD-1/CDK-4 expression also down-regulated a large number of genes enriched for catabolic functions. These results highlight distinct functions for the two G1 Cyclin/CDK complexes and reveal a previously unknown activity of Cyclin D/CDK-4 in regulating metabolic gene expression. Furthermore, our data demonstrate that many cell cycle genes can still be transcriptionally induced in post-mitotic muscle cells, while maintenance of the post-mitotic state might depend on stable repression of a limited number of critical cell cycle regulators

Aanpak droogte vraagt transitie waterbeheer

Jaarlijks ontvangt Nederland een hoeveelheid water die, bij een landoppervlak van 35.000 km2, overeenkomt met een waterschijf van ongeveer drie meter hoog. Ruim twee meter komt binnen via de rivieren en bijna een meter via de neerslag. Hiervan verdampt een halve meter, zodat er een surplus overblijft van 2,5 meter. Dat staat gelijk aan een watervolume van 88 miljard kuub. Toch kampen we in onze delta tijdens droge tijden met een watertekort, zoals we de afgelopen zomers hebben gemerkt

Rb and FZR1/Cdh1 determine CDK4/6-cyclin D requirement in C. elegans and human cancer cells

Cyclin-dependent kinases 4 and 6 (CDK4/6) in complex with D-type cyclins promote cell cycle entry. Most human cancers contain overactive CDK4/6-cyclin D, and CDK4/6-specific inhibitors are promising anti-cancer therapeutics. Here, we investigate the critical functions of CDK4/6-cyclin D kinases, starting from an unbiased screen in the nematode Caenorhabditis elegans. We found that simultaneous mutation of lin-35, a retinoblastoma (Rb)-related gene, and fzr-1, an orthologue to the APC/C co-activator Cdh1, completely eliminates the essential requirement of CDK4/6-cyclin D (CDK-4/CYD-1) in C. elegans. CDK-4/CYD-1 phosphorylates specific residues in the LIN-35 Rb spacer domain and FZR-1 amino terminus, resembling inactivating phosphorylations of the human proteins. In human breast cancer cells, simultaneous knockdown of Rb and FZR1 synergistically bypasses cell division arrest induced by the CDK4/6-specific inhibitor PD-0332991. Our data identify FZR1 as a candidate CDK4/6-cyclin D substrate and point to an APC/CFZR1 activity as an important determinant in response to CDK4/6-inhibitors

Rb and FZR1/Cdh1 determine CDK4/6-cyclin D requirement in C. elegans and human cancer cells

Cyclin-dependent kinases 4 and 6 (CDK4/6) in complex with D-type cyclins promote cell cycle entry. Most human cancers contain overactive CDK4/6-cyclin D, and CDK4/6-specific inhibitors are promising anti-cancer therapeutics. Here, we investigate the critical functions of CDK4/6-cyclin D kinases, starting from an unbiased screen in the nematode Caenorhabditis elegans. We found that simultaneous mutation of lin-35, a retinoblastoma (Rb)-related gene, and fzr-1, an orthologue to the APC/C co-activator Cdh1, completely eliminates the essential requirement of CDK4/6-cyclin D (CDK-4/CYD-1) in C. elegans. CDK-4/CYD-1 phosphorylates specific residues in the LIN-35 Rb spacer domain and FZR-1 amino terminus, resembling inactivating phosphorylations of the human proteins. In human breast cancer cells, simultaneous knockdown of Rb and FZR1 synergistically bypasses cell division arrest induced by the CDK4/6-specific inhibitor PD-0332991. Our data identify FZR1 as a candidate CDK4/6-cyclin D substrate and point to an APC/C(FZR1) activity as an important determinant in response to CDK4/6-inhibitors