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Sanchez and Dynlacht discuss recent insights into the mechanisms of primary cilia assembly and disassembly, and the relationships between ciliogenesis and cell cycle regulation as well as disease.
Tumour-associated macrophages facilitate cancer progression, but whether they can be reprogrammed to elicit an anti-tumour response remains unclear. Deletion of the microRNA-processing enzyme Dicer is now shown to rewire macrophages to an anti-tumour mode, leading to an enhanced response to immunotherapy and inhibition of tumour progression.
During development, tubular networks form through the joining of lumenized branches. Further insights into tracheal tube fusion in Drosophila melanogaster now reveal the molecular steps that promote the connection of two apical membrane compartments within a single cell through secretory lysosomes.
Although known to induce cellular senescence, an important tumour suppressor mechanism, mutation of CDKN1A — the gene encoding p21 (also known as WAF1 or CIP1) — is rare in human cancers. Now, a study reports a previously unappreciated oncogenic effect of p21 overexpression that shapes cancer genome evolution through induction of replication stress.
Clearing misfolded proteins from the cytoplasm is essential to maintain cellular homeostasis. Now, a parallel clearance system is described that uses the deubiquitylase USP19 to enable secretion of misfolded cytoplasmic proteins when conventional proteasomal degradation is compromised. Misfolding-associated protein secretion (MAPS) has important implications for protein quality control and prion-like transmission.
Luschnig and colleagues present a model in which Staccato, in combination with Rab39, mediates the control of apical membrane fusion by interacting with components of the SNARE machinery in the formation of anastomoses in the tracheal tube.
Kopito and Schrul show that the peroxisome proteins PEX19 and PEX3 mediate the correct insertion of the lipid droplet protein UBXD8 into ER subdomains.
Seokho et al. report that Wnt ligands bind the extracellular domain of polycystin 1 (PKD1) and induce Ca2+ influx through the Ca2+-permeable ion channel TRPP2. This activity is abrogated by PKD1 mutations linked to polycystic kidney disease.
Lee et al. report that aberrantly folded cytosolic proteins are recruited to the ER by the USP19 deubiquitylase, and are then encapsulated in late endosomes that fuse with the plasma membrane, leading to their secretion.
Galanos and colleagues observe p21 accumulation in proliferating cancer cells, and show that in cultured p53-null cells, p21 can cause genomic instability by perturbing replication licensing through inhibition of the CRL4-CDT ubiquitin ligase.
Baer et al. report that macrophage-specific DICER deletion abolishes TAM immunosuppressive activity and promotes anti-tumour immunity by recruitment and activation of cytotoxic T cells and increased IFN-γ production.
Banh et al. show that PTP1B decreases non-mitochondrial oxygen consumption by regulating the RNF213/α-KGDD pathway, thus promoting hypoxic survival of cancer cells.
By engineering mice to express a version of the Pten tumour suppressor that lacks the three C-terminal amino acids, van Deursen and colleagues reveal a role for the protein in the generation of symmetric spindles through recruitment of Eg5 to centrosomes.