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Tsatskis, Y.

Publications and source records attributed to Tsatskis, Y..

2 recordsLinked to original sources

Fat cadherin cleavage releases a transcriptionally active nuclear fragment to regulate target gene expression

The conserved atypical cadherin fat (ft) controls cellular processes such as growth, planar cell polarity, and mitochondrial function, in organisms ranging from fruit flies to mammals. Working at the apical-junctional plasma membrane the intracellular domain of the Ft protein, FtICD, binds to and regulates components of the Hippo and PCP pathways. Unexpectedly, we show that FtICD is present in the nucleus in cultured cells as well as in embryonic and larval tissues, and identify nuclear localization and nuclear export signals in FtICD required for this localization. We show that membrane-bound FtICD is cleaved and enters nuclei in vivo. Using endogenously tagged Ft as well as overexpressed FtICD we conducted ChIP-seq experiments and identified putative Ft targets including genes involved in signaling pathways, chromatin organization, pattern formation, and neural development. RNAseq demonstrates that some of these genes are differentially regulated in ft mutants. We observe strong correlations of Ft binding regions with peaks for other factors such as DREF and BEAF-32, as well as the Hpo pathway components Yorkie (Yki) and Scalloped (Sd), suggesting that Ft may act in conjunction with these factors to regulate gene expression. Supporting this hypothesis, we found that Ft can physically interact with both Yki and Sd in co-immunoprecipitation experiments in S2 cells. We propose that the modulation of Hippo pathway activity constitutes one of the nuclear functions of Ft, complementing its established function as an upstream regulator of Hippo signaling.

developmental biology↗

Mouse NEMP1 is required for erythropoiesis, nuclear envelope openings and enucleation of erythroblasts

Nuclear Envelope Membrane Proteins (NEMP) are a conserved family of nuclear envelope proteins that reside within the inner nuclear membrane. Even though Nemp1 knockout (KO) mice are overtly normal, they display a pronounced splenomegaly. This phenotype and recent reports describing a requirement for nuclear envelope openings during erythroblasts terminal maturation led us to examine a potential role for Nemp1 in erythropoiesis. Here, we report that Nemp1 knockout (KO) mice show peripheral blood defects, anemia in neonates, ineffective erythropoiesis, splenomegaly and stress erythropoiesis. The erythroid lineage of Nemp1 KO mice is overrepresented until the pronounced apoptosis of polychromatophilic erythroblasts. We show that NEMP1 localizes to the nuclear envelope of erythroblasts and their progenitors. Mechanistically, we discovered that NEMP1 accumulates into aggregates that localize near or at the edge of nuclear envelope openings and Nemp1 deficiency leads to a marked decrease of both nuclear envelope openings and ensuing enucleation. Together, our results for the first time demonstrate that NEMP1 is essential for nuclear envelope openings and erythropoietic maturation in vivo and provide the first mouse model of defective erythropoiesis directly linked to the loss of an inner nuclear membrane protein.

cell biology↗