Multifunctional BAF-1

N uclear assembly happens every cell division. So it's no surprise that nuclear assembly factors are overworked during embryogenesis, when proliferation is maximal. But there's no rest for one weary factor, called BAF-1, who has many jobs left to do even when embryogenesis is over, report Margalit et al. on page 661. BAF-1 is enriched at the nuclear periphery and is required for the capture of chromosomes in reforming nuclei. It binds to histones, DNA, and nuclear envelope proteins including lamin and emerin. Mutations to lamin and emerin, which are also crucial for nuclear assembly, somehow cause human diseases that manifest later in life, when cell division has lagged. In previous studies, the group found that knocking down the activity of BAF-1 in worms leads to embryonic death. They wondered, however, whether BAF-1, like lamin and emerin, might have functions later in life. To investigate this question, they used BAF-1– null worms that survived embryogenesis thanks to maternal BAF-1 supplies. These survivors displayed a diverse but reproducible array of tissue-specifi c defects. The defects suggested that BAF-1 promotes distal tip cell migration, muscle cell integrity, gonad and germline development , and the correct timing of epidermal seam cell fusion—a process that literally seals the worm's skin. BAF-1 delayed seam cell fusion by binding to the promoter and repressing the expression of the gene for a fusion factor called EFF-1. This newly described transcriptional regulatory activity might also explain BAF-1's other tissue-specific functions. Cellular career decisions start early T here's always one or two kids in every class who are already certain what they want to be when they grow up. Gerhart and colleagues now report on page 649 that certain cells of the early embryo are no different. The team is interested in how cells commit to becoming skeletal muscle, which requires the expression of a transcription factor called MyoD. This expression was thought to start in the somites. But George-Weinstein's group discovered that they could detect MyoD mRNA in the blastocyst—a whole day before somites form, when cells are thought to be still pluripotent. MyoD-expressing cells isolated from the blastocyst were capable of differentiating into skeletal muscle in culture. This ability did not mean, however, that the cells were already committed to muscle differentiation. It was possible that the MyoD mRNA was nonfunctional. Indeed, no MyoD protein was detectable at this stage. To investigate whether MyoD-positive blastocyst cells were …