The Osiris family genes function as novel regulators of the tube maturation process in the Drosophila trachea.

Drosophila trachea is a premier model to study tube morphogenesis. After the formation of continuous tubes, tube maturation follows. Tracheal tube maturation starts with an apical secretion pulse that deposits extracellular matrix components to form a chitin-based apical luminal matrix (aECM). This aECM is then cleared and followed by the maturation of taenidial folds. Finally, air fills the tubes. Meanwhile, the cellular junctions are maintained to ensure tube integrity. Previous research has identified several key components (ER, Golgi, several endosomes) of protein trafficking pathways that regulate the secretion and clearance of aECM, and the maintenance of cellular junctions. The Osiris (Osi) gene family is located at the Triplo-lethal (Tpl) locus on chromosome 3R 83D4-E3 and exhibits dosage sensitivity. Here, we show that three Osi genes (Osi9, Osi15, Osi19), function redundantly to regulate adherens junction (AJ) maintenance, luminal clearance, taenidial fold formation, tube morphology, and air filling during tube maturation. The localization of Osi proteins in endosomes (Rab7-containing late endosomes, Rab11-containing recycling endosomes, Lamp-containing lysosomes) and the reduction of these endosomes in Osi mutants suggest the possible role of Osi genes in tube maturation through endosome-mediated trafficking. We analyzed tube maturation in zygotic rab11 and rab7 mutants, respectively, to determine whether endosome-mediated trafficking is required. Interestingly, similar tube maturation defects were observed in rab11 but not in rab7 mutants, suggesting the involvement of Rab11-mediated trafficking, but not Rab7-mediated trafficking, in this process. To investigate whether Osi genes regulate tube maturation primarily through the maintenance of Rab11-containing endosomes, we overexpressed rab11 in Osi mutant trachea. Surprisingly, no obvious rescue was observed. Thus, increasing endosome numbers is not sufficient to rescue tube maturation defects in Osi mutants. These results suggest that Osi genes regulate other aspects of endosome-mediated trafficking, or regulate an unknown mechanism that converges or acts in parallel with Rab11-mediated trafficking during tube maturation.

Use-dependent and error-based learning of motor behaviors.

Human motor behavior is constantly adapted through the process of error-based learning. When the motor system encounters an error, its estimate about the body and environment will change, and the next movement will be immediately modified to counteract the underlying perturbation. Here, we show that a second mechanism, use-dependent learning, simultaneously changes movements to become more similar to the last movement. In three experiments, participants made reaching movements toward a horizontally elongated target, such that errors in the initial movement direction did not have to be corrected. Along this task-redundant dimension, we were able to induce use-dependent learning by passively guiding movements in a direction angled by 8 degrees from the previous direction. In a second study, we show that error-based and use-dependent learning can change motor behavior simultaneously in opposing directions by physically constraining the direction of active movements. After removal of the constraint, participants briefly exhibit an error-based aftereffect against the direction of the constraint, followed by a longer-lasting use-dependent aftereffect in the direction of the constraint. In the third experiment, we show that these two learning mechanisms together determine the solution the motor system adopts when learning a motor task.