Daughter cells share duties

Mitochondrial DNA stays home M itochondria stow their DNA in structures called nucleoids. As Gilkerson et al. reveal, nucleoids are selfi sh and don’t share their DNA with each other. The results might help explain some quirks of mitochondrial inheritance and support a proposed treatment strategy for illnesses caused by defects in the organelles. A nucleoid can house up to 10 copies of a mitochondrion’s genome. One reason that the structures intrigue researchers is that they might help control how the DNAs get parceled out when mitochondria divide. To understand mitochondrial DNA inheritance, researchers need to resolve whether nucleoids swap DNA. The question has remained unanswered because of the diffi culty of tracking individual mitochondrial DNAs. To overcome that problem, Gilkerson et al. fused two kinds of cells, each of which carried a different mitochondrial genome. In the merged cells, the researchers found, labeled versions of the two types of mitochondrial DNA rarely appeared together, suggesting that the nucleoids weren’t mingling their contents. Stingy nucleoids could explain why cells that harbor a variety of mitochondrial genomes sometimes lose DNA diversity as they divide and sometimes don’t. The outcome might depend on whether the DNAs in a particular nucleoid are uniform or varied. The results also offer support for plans to treat mitochondrial diseases by nudging cells to eliminate defective DNA. The lack of swapping will make it easier to purge faulty mitochondrial genomes, the researchers say. Gilkerson, R.W., et al. 2008. J. Cell Biol. doi:10.1083/jcb.200712101. How cells make local calls B roadcast a message over a loudspeaker, and you can’t be sure who will hear it. But whisper the message into the friend’s ear, and you can be sure it got through. Cells follow a similar strategy when they transmit signals with reactive oxygen species (ROS), as Chen et al. show. By positioning the sender and recipient molecules near each other, cells ensure effi cient communication. ROS are best known as destructive byproducts of metabolism that might cause aging. But cells also use the molecules to carry messages. The mystery is how cells direct ROS to their targets, since some ROS can diffuse throughout the cell, potentially reacting with any molecules they encounter. Proximity is the key, Chen et al. found. They tracked down the signalrelaying molecule NADPH oxidase 4 (Nox4), which produces the ROS hydrogen peroxide. The protein was stationed in the endoplasmic reticulum near another protein called PTP1B, which slows division of endothelial cells by turning down the epidermal growth factor receptor (EGFR). The team showed that Nox4 was oxidizing and shutting down adjacent PTP1B molecules. Using an antioxidant that homes in on the ER, for instance, the team could block EGFR signaling, indicating that oxidation of PTP1B had been prevented. An antioxidant that remains in the cytoplasm, however, had no effect on the receptor. The results suggest that by keeping Nox4 and PTP1B close together in the ER, cells make it easier for ROS signals to travel between them. One question the researchers now want to answer is what activates Nox4 in the fi rst place. Chen, K., et al. 2008. J. Cell Biol. doi:10.1083/jcb.200709049. Daughter cells share duties T here’s no sibling rivalry during cell division. Goss and Toomre show that during cytokinesis both daughter cells pitch in to supply new membrane. Researchers suspect that during cytokinesis, fresh membrane shuttles to the junction between the two daughter cells. Where the membrane comes from has puzzled researchers. A previous study using spinning disc confocal microscopy suggested that only one daughter cell provides it. However, that study didn’t track individual membrane vesicles. Goss and Toomre were able to do just that by capturing images 60 times faster. They found that vesicles from both daughter cells leave the Golgi apparatus and cruise to the cleavage furrow, accumulating there. Although other potential sources of membrane, including endosomes, also collect near the furrow, they remain aloof from the Golgi-derived vesicles that will ultimately fuse with the cell membrane. With total internal refl ection fl uorescence microscopy, the team observed individual vesicles from both daughter cells merging with the plasma membrane at the cleavage furrow. However, the results don’t necessarily confl ict with the previous study, the researchers say. They note that they also observed an asymmetric stage in which only one cell appears to direct vesicles to the cleavage furrow. Goss, J.W., and D.K. Toomre. 2008. J. Cell Biol. doi:10.1083/jcb.200712137. Golgi-derived vesicles (green) amass at the cleavage furrow.