Faculty Bibliography

Early hominins formed large and thick-enamelled cheek-teeth within relatively short growth periods as compared with modern humans. To understand better the developmental basis of this process, we measured daily enamel increments, or cross striations, in 17 molars of Plio-Pleistocene hominins representing seven different species, including specimens attributed to early Homo. Our results show considerable variation across species, although all specimens conformed to the known pattern characterised by greater values in outer than inner enamel, and greater cuspal than cervical values. We then compared our results with the megadontia index, which represents tooth size in relation to body mass, for each species to assess the effect of daily growth rates on tooth size. Our results indicate that larger toothed (megadont) taxa display higher rates or faster forming enamel than smaller toothed hominins. By forming enamel quickly, large tooth crowns were able to develop within the constraints of shorter growth periods. Besides daily increments, many animals express long-period markings (striae of Retzius) in their enamel. We report periodicity values (number of cross striations between adjacent striae) in 14 new specimens of Australopithecus afarensis, Paranthropus aethiopicus, Paranthropus boisei, Homo habilis, Homo rudolfensis and Homo erectus, and show that long-period striae express a strong association with male and average male-female body mass. Our results for Plio-Pleistocene hominins show that the biological rhythms that give rise to long-period striae are encompassed within the range of variation known for modern humans, but show a lower mean and modal value of 7 days in australopithecines. In our sample of early Homo, mean and modal periodicity values were 8 days, and therefore similar to modern humans. These new data on daily rates of enamel formation and periodicity provide a better framework to interpret surface manifestations of internal growth markings on fossil hominin tooth crowns. Importantly, our data on early hominin cross striation variation may now contribute towards solving difficult taxonomic diagnoses where much may depend on fragmentary molar remains and enamel structure.

OBJECTIVE: Our objective is to exploit architectural constraint for the analysis and interpretation of craniofacial form, which we apply here to the reconstruction of the early Homo cranium KNM-ER 1470. We are motivated to perform this study because in the absence of biological criteria our preconceptions are likely to govern our concept of craniofacial form. STUDY DESIGN: We reassembled the fragmented parts--left and right halves of the calvaria and the face--according to mammalian craniofacial architectural constraints described by Donald H. Enlow and colleagues. RESULTS: When evaluated on a biological premise, KNM-ER 1470 is found to have a more prognathic midface than commonly appreciated. The relationship between facial prognathism and cranial capacity also provides an estimate downward for this specimen, from 752cc to ca. 700cc. CONCLUSION: Awareness of our preconceptions is critical to the performance of relatively unbiased research in fields characterized by interpretations of morphology. When perceptual bias is relatively minimized, applied here as an architecturally constrained of KNM-ER 1470 craniofacial skeleton, we are able to provide the scientific community with a more tractable Gestalt perspective of form

Pocket proteins and cyclin-dependent kinase (CDK) inhibitors negatively regulate cell proliferation and can promote differentiation. However, which members of these gene families, which cell type they interact in, and what they do to promote differentiation in that cell type during mouse development are largely unknown. To identify the cell types in which p107 and p27 interact, we generated compound mutant mice. These mice were null for p107 and had a deletion in p27 that prevented its binding to cyclin-CDK complexes. Although a fraction of these animals survived into adulthood and looked similar to single p27 mutant mice, a larger number of animals died at birth or within a few weeks thereafter. These animals displayed defects in chondrocyte maturation and endochondral bone formation. Proliferation of chondrocytes was increased, and ectopic ossification was observed. Uncommitted mouse embryo fibroblasts could be induced into the chondrocytic lineage ex vivo, but these cells failed to mature normally. These results demonstrate that p27 carries out overlapping functions with p107 in controlling cell cycle exit during chondrocyte maturation. The phenotypic similarities between p107(-/-) p27(D51/D51) and p107(-/-) p130(-/-) mice and the cells derived from them suggest that p27 and p130 act in an analogous pathway during chondrocyte maturation