Coupled whole-body rhythmic entrainment between two chimpanzees

Dance is an icon of human expression. Despite astounding diversity around the world’s cultures and dazzling abundance of reminiscent animal systems, the evolution of dance in the human clade remains obscure. Dance requires individuals to interactively synchronize their whole-body tempo to their partner’s, with near-perfect precision. This capacity is motorically-heavy, engaging multiple neural circuitries, but also dependent on an acute socio-emotional bond between partners. Hitherto, these factors helped explain why no dance forms were present amongst nonhuman primates. Critically, evidence for conjoined full-body rhythmic entrainment in great apes that could help reconstruct possible proto-stages of human dance is still lacking. Here, we report an endogenously-effected case of ritualized dance-like behaviour between two captive chimpanzees – synchronized bipedalism. We submitted video recordings to rigorous time-series analysis and circular statistics. We found that individual step tempo was within the genus’ range of “solo” bipedalism. Between-individual analyses, however, revealed that synchronisation between individuals was non-random, predictable, phase concordant, maintained with instantaneous centi-second precision and jointly regulated, with individuals also taking turns as “pace-makers”. No function was apparent besides the behaviour’s putative positive social affiliation. Our analyses show a first case of spontaneous whole-body entrainment between two ape peers, thus providing tentative empirical evidence for phylogenies of human dance. Human proto-dance, we argue, may have been rooted in mechanisms of social cohesion among small groups that might have granted stress-releasing benefits via gait-synchrony and mutual-touch. An external sound/musical beat may have been initially uninvolved. We discuss dance evolution as driven by ecologically-, socially- and/or culturally-imposed “captivity”

Regulation of splicing networks in neurodevelopment

Alternative splicing of pre-mRNA is a critical mechanism for enabling genetic diversity, and is a carefully regulated process in neuronal differentiation. RNA binding proteins (RBPs) are developmentally expressed and physically interact with RNA to drive specific splicing changes. This work tests the hypothesis that RBP-RNA interactions are critical for regulating timed and coordinated alternative splicing changes during neurodevelopment and that these splicing changes are in turn part of major regulatory mechanisms that underlie morphological and functional maturation of neurons. I describe our efforts to identify functional RBP-RNA interactions, including the identification of previously unobserved splicing events, and explore the combinatorial roles of multiple brain-specific RBPs during development. Using integrative modeling that combines multiple sources of data, we find hundreds of regulated splicing events for each of RBFOX, NOVA, PTBP, and MBNL. In the neurodevelopmental context, we find that the proteins control different sets of exons, with RBFOX, NOVA, and PTBP regulating early splicing changes and MBNL largely regulating later splicing changes. These findings additionally led to the observation that CNS and sensory neurons express a variety of different RBP programs, with many sensory neurons expressing a less mature splicing pattern than CNS neurons. We also establish a foundation for further exploration of neurodevelopmental splicing, by investigating the regulation of previously unobserved splicing events

On the role of molecular mechanisms and unequal cleavage during neurogenesis in the C. elegans C lineage

Required for neurogenesis is a family of evolutionarily conserved bHLH transcription factors known as proneural genes. However, regulation of their initial expression remains a poorly understood aspect of neurodevelopment in any model, particularly Caenorhabditis elegans. A key mechanism by which cells acquire different fates is asymmetric division and in neuronal lineages these often generate unequally sized daughters. Whether this unequal size directly affects cell fate regulation is often unknown. Indeed, the question of how control of cell size intersects with fate decisions is poorly understood in biology more generally. Taking advantage of the single-cell resolution provided by the invariant cell lineage of C. elegans, I interrogate these two fundamental biological questions in the C lineage. Expression of the proneural gene hlh-14/Ascl1 in a single branch of the lineage is required for neurogenesis of the DVC and PVR neurons and is immediately preceded by unequal cleavages. Addressing both molecular and cellular regulators I perform a 4D-lineage based genetic screen for upstream regulators of hlh-14/Ascl1 and address the effect of unequal cleavage and daughter cell size. I find that a regulator of other neuronal lineage cleavages, PIG-1/MELK, is also required in the C lineage, yet equalisation does not affect the initiation of hlh-14/Ascl1 expression. Conversely, I demonstrate that unequal cleavage and acquisition of neuronal fate in separate successive divisions are controlled by the same key regulators. The first by an upstream regulator of hlh-14, the Mediator complex kinase module let-19/Mdt-13 and the second by hlh-14 itself. Taken together the results described in this thesis suggest that rather than acting to correctly segregate initial proneural gene expression, unequal cleavages are instead co-regulated by the same factors regulating neuronal fate acquisition. This co-regulation at successive divisions thus coordinates two separable aspects of fate; acquisition of neuronal identity and correct post-mitotic embryonic cell size