Trypanosomes show their commitment

Pek et al. describe how a stable, intron-derived RNA regulates the expression of its host gene during Drosophila embryogenesis. Once they are spliced out of nascent mRNAs, noncoding intron sequences are usually degraded rapidly. At least in Xenopus eggs and human cell lines, however, some intronic RNAs persist for long periods, although the function of these stable intronic sequence (sis) RNAs remains unknown. Pek et al. used deep sequencing to look for sisRNAs in newly fertilized Drosophila embryos, whose initial development depends on a pool of stable RNA generated several hours earlier during oogenesis. The researchers identifi ed over 30 candidate sisRNAs, including one, dubbed sisR-1, that was derived from the fourth intron of a gene called rga. After being spliced out of the rga pre-mRNA, sisR-1 was processed into longer and shorter versions that localized to the nucleus and cytoplasm, respectively. Structural predictions suggested that the 3′ region of nuclear sisR-1 is exposed and available to base pair with an antisense transcript, named ASTR, that is also produced from the rga locus. Pek et al. discovered that ASTR promoted transcription of the rga gene in early embryos, causing sisR-1 to gradually accumulate until, later in development, it was able to suppress ASTR and shut down rga expression. Knocking down sisR-1 delayed the down-regulation of ASTR and rga, but otherwise embryogenesis proceeded normally. Senior author Jun Wei Pek now wants to investigate how sisR-1 is stabilized, and whether its knockdown affects fl y development in sensitized genetic backgrounds. Lammers and Markus describe how dynein is activated at the budding yeast cell cortex so that it can pull on astral mi-crotubules and position the mitotic spindle. During mitosis, dy-nein motors are anchored at the yeast cell cortex by the receptor protein Num1. Dynein is transferred to Num1 from the plus ends of dynamic astral microtubules. Pac1 (a homologue of human LIS1) links dynein to the plus-end tracking protein Bik1 and prevents the motor from prematurely walking away toward the microtubule minus end. Once anchored to Num1, though, dynein's minus end–directed motility is activated and the mitotic spindle is pulled into the bud. Whether Num1 directly activates dynein is unknown, however. Lammers and Markus found that overexpressing the dynein-binding domain of Num1 prompted the motor protein's premature disappearance from astral microtubule plus ends. Live imaging of cells expressing this Num1 domain showed dynein moving toward micro-tubule minus ends attached to the yeast …