Building modular motor complexes

Satellite RNA guides kinetochore assembly R ošić et al. reveal that a non-coding RNA transcribed from repetitive DNA sequences promotes kinetochore assembly and chromosome segregation during mitosis. Centromeres—the chromosome regions where kinetochore proteins assemble and attach chromosomes to the mitotic spindle—are defi ned by epige-netic factors such as the histone variant CENP-A rather than by their specific DNA sequence. Centromeric chromatin is often characterized, however , by the presence of repetitive DNA sequences called satellite repeats , and some evidence suggests that RNAs transcribed from these regions might help cells identify the location of their centromeres. Rošić et al. found that noncoding RNA transcribed from the satellite III (SAT III) repeats on the Drosophila X chromosome localized to the centromeres of most mitotic chromosomes. Depleting these SAT III transcripts caused defects in the segregation of all these chromosomes, not just the X chromosome. The researchers frequently saw chromosomes that failed to move to the spindle poles during anaphase. These lagging chromosomes showed reduced levels of centromere and kinetochore proteins including CENP-A, CENP-C, and Spc105, indicating that they are unable to attach to the mitotic spindle correctly. SAT III transcripts interacted with CENP-C, suggesting that the RNA helps to recruit or stabilize this protein at centro-meres, thereby promoting CENP-A incorporation and kinetochore assembly. Senior author Sylvia Erhardt thinks that noncoding RNAs transcribed from other satellite repeats may similarly act as epigenetic markers of centromeres. She now wants to investigate how SAT III transcription is regulated and to determine how the RNA interacts with CENP-C. mTORC2 helps brown adipose tissue fuel up T he kinase complex mTORC2 is the key regulator for adreno-ceptor-stimulated glucose uptake in brown adipocytes, Olsen et al. reveal. Brown adipose tissue can take up large amounts of glucose from the bloodstream to use as a fuel source to generate body heat. The sympathetic nervous system stimulates glucose uptake by activating the ␤ 3-adrenoceptor, but the signaling pathway leading to GLUT1-dependent glucose import is largely unknown. Insulin induces glucose uptake by activating the kinases PI3K and Akt, but Olsen et al. found that inhibiting these kinases had no effect on ␤ 3-adrenoceptor–stimulated glucose import. In contrast, inhibiting the mTOR kinase—a key regulator of cell metabolism— blocked glucose uptake in both mouse and human adipocytes in response to ␤ 3-adrenoceptor activation. mTOR inhibitors had no effect on cAMP-dependent GLUT1 expression but impaired the transporter's subsequent delivery to the plasma membrane. …