A modern human pattern of dental development in Lower Pleistocene hominids from Atapuerca-TD6 (Spain)

The study of life history evolution in hominids is crucial for the discernment of when and why humans have acquired our unique maturational pattern. Because the development of dentition is critically integrated into the life cycle in mammals, the determination of the time and pattern of dental development represents an appropriate method to infer changes in life history variables that occurred during hominid evolution. Here we present evidence derived from Lower Pleistocene human fossil remains recovered from the TD6 level (Aurora stratum) of the Gran Dolina site in the Sierra de Atapuerca, northern Spain. These hominids present a pattern of development similar to that of Homo sapiens, although some aspects (e.g., delayed M3 calcification) are not as derived as that of European populations and people of European origin. This evidence, taken together with the present knowledge of cranial capacity of these and other late Early Pleistocene hominids, supports the view that as early as 0.8 Ma at least one Homo species shared with modern humans a prolonged pattern of maturation.

Statistical analysis of shape through triangulation of landmarks: A study of sexual dimorphism in hominids

Two objects with homologous landmarks are said to be of the same shape if the configuration of landmarks of one object can be exactly matched with that of the other by translation, rotation/reflection, and scaling. In an earlier paper, the authors proposed statistical analysis of shape by considering logarithmic differences of all possible Euclidean distances between landmarks. Tests of significance for differences in the shape of objects and methods of discrimination between populations were developed with such data. In the present paper, the corresponding statistical methodology is developed by triangulation of the landmarks and by considering the angles as natural measurements of shape. This method is applied to the study of sexual dimorphism in hominids.

Appendicular robusticity and the paleobiology of modern human emergence

The emergence of modern humans in the Late Pleistocene, whatever its phylogenetic history, was characterized by a series of behaviorally important shifts reflected in aspects of human hard tissue biology and the archeological record. To elucidate these shifts further, diaphyseal cross-sectional morphology was analyzed by using cross-sectional areas and second moments of area of the mid-distal humerus and midshaft femur. The humeral diaphysis indicates a gradual reduction in habitual load levels from Eurasian late archaic, to Early Upper Paleolithic early modern, to Middle Upper Paleolithic early modern hominids, with the Levantine Middle Paleolithic early modern humans being a gracile anomalous outlier. The femoral diaphysis, once variation in ecogeographically patterned body proportions is taken into account, indicates no changes across the pre-30,000 years B.P. samples in habitual locomotor load levels, followed by a modest decrease through the Middle Upper Paleolithic.

WIP, a protein associated with Wiskott–Aldrich syndrome protein, induces actin polymerization and redistribution in lymphoid cells

Wiskott–Aldrich syndrome (WAS) is an X-linked immunodeficiency caused by mutations that affect the WAS protein (WASP) and characterized by cytoskeletal abnormalities in hematopoietic cells. By using the yeast two-hybrid system we have identified a proline-rich WASP-interacting protein (WIP), which coimmunoprecipitated with WASP from lymphocytes. WIP binds to WASP at a site distinct from the Cdc42 binding site and has actin as well as profilin binding motifs. Expression of WIP in human B cells, but not of a WIP truncation mutant that lacks the actin binding motif, increased polymerized actin content and induced the appearance of actin-containing cerebriform projections on the cell surface. These results suggest that WIP plays a role in cortical actin assembly that may be important for lymphocyte function.

Evidence of termite foraging by Swartkrans early hominids

Previous studies have suggested that modified bones from the Lower Paleolithic sites of Swartkrans and Sterkfontein in South Africa represent the oldest known bone tools and that they were used by Australopithecus robustus to dig up tubers. Macroscopic and microscopic analysis of the wear patterns on the purported bone tools, pseudo bone tools produced naturally by known taphonomic processes, and experimentally used bone tools confirm the anthropic origin of the modifications. However, our analysis suggests that these tools were used to dig into termite mounds, rather than to dig for tubers. This result indicates that early hominids from southern Africa maintained a behavioral pattern involving a bone tool material culture that may have persisted for a long period and strongly supports the role of insectivory in the early hominid diet.

A missense mutation of the Na+ channel αII subunit gene Nav1.2 in a patient with febrile and afebrile seizures causes channel dysfunction

Generalized epilepsy with febrile seizures plus (GEFS+), a clinical subset of febrile seizures (FS), is characterized by frequent episodes beyond 6 years of age (FS+) and various types of subsequent epilepsy. Mutations in β1 and αI-subunit genes of voltage-gated Na+ channels have been associated with GEFS+1 and 2, respectively. Here, we report a mutation resulting in an amino acid exchange (R187W) in the gene encoding the α-subunit of neuronal voltage-gated Na+ channel type II (Nav1.2) in a patient with FS associated with afebrile seizures. The mutation R187W occurring on Arg187, a highly conserved residue among voltage-gated Na+ channels, was not found in 224 alleles of unaffected individuals. Whole-cell patch clamp recordings on human embryonic kidney (HEK) cells expressing a rat wild-type (rNav1.2) and the corresponding mutant channels showed that the mutant channel inactivated more slowly than wild-type whereas the Na+ channel conductance was not affected. Prolonged residence in the open state of the R187W mutant channel may augment Na+ influx and thereby underlie the neuronal hyperexcitability that induces seizure activity. Even though a small pedigree could not show clear cosegregation with the disease phenotype, these findings strongly suggest the involvement of Nav1.2 in a human disease and propose the R187W mutation as the genetic defect responsible for febrile seizures associated with afebrile seizures.