The death stops here

The death stops here lants rely on a sensitive process of programmed cell death to curtail pathogenic infection by selectively executing infected cells. To prevent the death response from spreading to noninfected areas, cells near and at the site of infection activate autophagy, say and colleagues. In virus-infected plants that are unable to turn on autophagy, cell death spreads from the site of infection to surrounding healthy tissues and even to adjacent leaves. " The programmed cell death response is very discrete, and we were interested in answering the question of what makes death stop, " says Dinesh-Kumar. To that end, the team used RNAi to identify genes involved in disease resistance and the programmed cell death response. They struck death paydirt when they silenced BECLIN1 , a gene that has been implicated in autophagy based on its abilities to rescue autophagy-defective P Plant cells generate autolysosomes (green) following viral infection to limit the spread of cell death. yeast and to prevent premature senescence in plants. Whether the plant was attacked by viral, bacterial, or fungal pathogens, BECLIN1 and other autophagy genes limited pathogen-induced cell death to the infection site and also repressed viral replication. These findings contrast with the situation in mammalian cells, where autophagy genes are required for initiating programmed cell death when apoptotic machinery is compromised. Autophagy may promote cell survival by controlling the production of the pro-death signal, preventing the movement of the signal into uninfected cells, or protecting cells against cellular damage caused in defense against pathogenic invasion. The group also discovered that the spreading pro-death signal does not arise from the virus itself. Sites of virus infection within leaves did not expand despite extensive cellular death throughout the plant, and plants infected with just the viral protein that elicits the programmed cell death response still showed widespread cell execution despite the viral protein's inability to move. The big mystery, and a new focus for Dinesh-Kumar's research, therefore centers on identifying this mobile pro-death signal and its origin. uring mitosis, the absence of Ran-GTPase pathway components at kinetochores leads to aberrant attachment of kinetochore fibers, disordered mitotic spindle assembly, and haphazard chromosome segregation at anaphase. To ensure that Ran complex proteins get where they need to be, Crm1—the Ran-GTP– binding nuclear export receptor—goes moonlighting at kinetochores after nuclear envelope breakdown, according to Alexei Arnaoutov, Mary Dasso (National Institute of Child Health and Human Development, Bethesda, …