Is automatic imitation a specialized form of stimulus–response compatibility? Dissociating imitative and spatial compatibilities

In recent years research on automatic imitation has received considerable attention because it represents an experimental platform for investigating a number of inter-related theories suggesting that the perception of action automatically activates corresponding motor programs. A key debate within this research centers on whether automatic imitation is any different than other long-term S-R associations, such as spatial stimulus-response compatibility. One approach to resolving this issue is to examine whether automatic imitation shows similar response characteristics as other classes of stimulus-response compatibility. This hypothesis was tested by comparing imitative and spatial compatibility effects with a two alternative forced-choice stimulus-response compatibility paradigm and two tasks: one that involved selecting a response to the stimulus (S-R) and one that involved selecting a response to the opposite stimulus (OS-R), i.e., the one not presented. The stimulus for both tasks was a left or right hand with either the index or middle finger tapping down. Speeded responses were performed with the index or middle finger of the right hand in response to the finger identity or the left-right spatial position of the fingers. Based on previous research and a connectionist model, we predicted standard compatibility effects for both spatial and imitative compatibility in the S-R task, and a reverse compatibility effect for spatial compatibility but not for imitative compatibility in the OS-R task. The results from the mean response times, mean percentage of errors, and response time distributions all converged to support these predictions. A second noteworthy result was that the recoding of the finger identity in the OS-R task required significantly more time than the recoding of the left-right spatial position, but the encoding time for the two stimuli in the S-R task was equivalent. In sum, this evidence suggests that the processing of spatial and imitative compatibility is dissociable with regard to two different processes in dual processing models of stimulus-response compatibility

Integrated genome-wide chromatin occupancy and expression analyses identify key myeloid pro-differentiation transcription factors repressed by Myb

To gain insight into the mechanisms by which the Myb transcription factor controls normal hematopoiesis and particularly, how it contributes to leukemogenesis, we mapped the genome-wide occupancy of Myb by chromatin immunoprecipitation followed by massively parallel sequencing (ChIP-Seq) in ERMYB myeloid progenitor cells. By integrating the genome occupancy data with whole genome expression profiling data, we identified a Myb-regulated transcriptional program. Gene signatures for leukemia stem cells, normal hematopoietic stem/progenitor cells and myeloid development were overrepresented in 2368 Myb regulated genes. Of these, Myb bound directly near or within 793 genes. Myb directly activates some genes known critical in maintaining hematopoietic stem cells, such as Gfi1 and Cited2. Importantly, we also show that, despite being usually considered as a transactivator, Myb also functions to repress approximately half of its direct targets, including several key regulators of myeloid differentiation, such as Sfpi1 (also known as Pu.1), Runx1, Junb and Cebpb. Furthermore, our results demonstrate that interaction with p300, an established coactivator for Myb, is unexpectedly required for Myb-mediated transcriptional repression. We propose that the repression of the above mentioned key pro-differentiation factors may contribute essentially to Myb’s ability to suppress differentiation and promote self-renewal, thus maintaining progenitor cells in an undifferentiated state and promoting leukemic transformation