Deacetylase undoes DNA damage

n page 993, Bucciarelli et al. report the first evidence that chromosomes are not always necessary for proper spindle assembly and cell division. The authors stumbled upon chromosome-independent cell division during a screen for meiosis mutants in Drosophila. Two of the mutants they identified, fusolo and solofuso , had chromosome segregation defects that led to secondary spermato-cytes lacking chromosomes. Nonetheless, these male germ cells constructed normal centrosome-nucleated astral arrays and a typical central spindle, appropriately containing the cell cleavage protein Aurora B. A contractile ring including the usual components of the cytokinetic apparatus (such as F-actin and myosin II) formed around the midzone in the mutants, and cytokinesis progressed as in wild-type cells. Unlike in fly spermatocytes, in all other systems studied so far, including fly and frog embryonic cells and mouse female gametes, spindle formation and progression to telophase is blocked in the absence of chromosomes. The authors of the current study can only speculate about what gives fly meiosis this unique twist. Perhaps a chromosome-independent division apparatus was a response to the particularly high ratio of microtubules to DNA in fly male meiotic spindles. Or possibly, as more cell types are examined, chromosome-free cytokinesis will be found in other systems. Either way, the findings indicate that the high concentrations of RanGTP found at chromosomes are not always necessary for spindle formation and progression to telophase, and that the interaction of microtubules emanating from two opposing asters might sometimes be enough. ᭿ O DNA (blue) is not essential (right) for normal spindle assembly and division (top to bottom) in fly germ cells. stores he endoplasmic reticulum (ER) converses with mitochondria during apoptosis, as reported on page 1115. The article by Breckenridge et al. identifies Ca21 as an interorganel-lar signal that sensitizes mitochondria to death-inducing injuries. The link between ER-associated events and mitochondrial remodeling during cell death lies in the BAP31 protein, an integral ER membrane protein that is a target of caspase-8. Previous studies indicated that full-length BAP31 inhibits mitochondrial release of cyt c during apoptosis, whereas overexpression of BAP31's caspase cleavage product, p20, induces cell death. The current study demonstrates that p20 exerts its apoptosis-inducing activity from the ER by inducing mitochondrial fission. ER and mitochondria were found to communicate through an exchange of Ca 2 ϩ. Expression of p20 induced Ca 2 ϩ release from the ER and near simultaneous Ca 2 ϩ uptake into the mitochondria. …