L. Bryan Ray

STKE: Steroid-Induced Motility

STKE New studies of the migration of specialized follicle cells known as border cells in Drosophila point to an unexpected role for steroid hormones in control of cell motility. In a screen for mutations that disrupted border cell migration, Bai et al. identified mutations in a gene they call taiman

Hypo)Nasty Plant Mutation

STKE A mutation in Arabidopsis may help define a role for double-stranded RNA binding proteins in mediating signals from multiple plant hormones. Lack of function of the HYPONASTIC (meaning movement bending the leaves inward and upward) LEAVES protein (HYL1) leads to a pleiotropic phenotype

Facilitator for Carcinogenesis

STKE To grow and become invasive, tumor cells solicit aid from other cells, such as the vascular endothelial cells that form new blood vessels in the tissues that the cancer cells invade. Bergers et al . used a transgenic mouse model of multistage carcinogenesis to analyze the onset of angiogenesis

STKE: Isomer-Specific Dephosphorylation

STKE The protein Pin1 is an isomerase that catalyzes interconversion of cis and trans forms of proline in polypeptides and is thought to function in signaling pathways that control cell division. Zhou et al . propose a mechanism by which Pin1 might influence signaling through such pathways. They report that the proline-directed phosphatase known as protein phosphatase 2A (PP2A) is stereospecific and dephosphorylates only trans phosphoSer- or phosphoThr-Pro peptides; Pin1 may function to facilitate dephosphorylation of potential PP2A substrates by promoting cis-trans isomerization. Consistent with this possibility, genetic evidence indicates that overexpression of Pin1 can partially overcome defects caused by conditional mutations in PP2A, and defects from loss of Pin1 function are reduced in cells overexpresssing PP2A. — LBR Mol. Cell 6, 873 (2000).

STKE: Restoring Retinoid Signals in Cancer Cells

STKE Retinoids have multiple biological effects, including inhibition of proliferation of certain cancer cells. The retinoids often act through heterodimers of two nuclear receptors, the retinoic acid receptors (RARs) and the retinoid X receptors (RXRs). In normal cells, the expression of RARb is enhanced through transcriptional activation in response to retinoids, but many cancer cell lines lose their ability to response even though the RAR and RXR proteins are still expressed. Lin et al. now show that such retinoid-insensitive cells may be missing another nuclear receptor, the orphan receptor COUP-TF. In cancer cell lines lacking COUP-TF, expression of COUP-TF restored retinoid-induced expression of RARb as well as the apoptotic and growth inhibitory effects of retinoic acid in these cells. COUP-TF appears to enhance the interaction of RAR with the transcriptional coactivator CBP through DNA binding. This mechanism of action of COUP-TF is distinct from its effects on other genes, where it has its own transactivation activity through recruitment of a different coactivator.— LBR Mol. Cell. Biol. 20 , 957 (2000).