Lumbar lordosis is the most critical element of human bipedality, because it obviates reliance on a bent-hip-bent-knee gait as practiced by African apes. The latter lack lumbar mobility because their most caudal lumbars are trapped by dorsally extended ilia. Early hominids show an opposite state—emancipation of their most caudal lumbar by reduced iliac height and expansion of sacral breadth. Could these anatomical shifts have been our earliest adaptations to upright walking? Are their parallels in other primates?
New World atelines use their prehensile tails for suspension, which also induces lordosis. Their pelves and lumbar columns show striking parallels with those of hominids, suggesting a parallel origin of this unusual adaptation.
HoxD11 partially determines the position of the lumbosacral transition, which might bear on this issue. In mouse, a bipartite enhancer controls its spatiotemporal expression. I examined a possible correlation between HoxD11 enhancer variation and lumbar column length by amplifying, cloning, and sequencing its bipartite enhancer in multiple species. Newly generated sequences were analyzed with published orthologs of several other primates, mouse, and zebrafish. New World monkeys appear to exhibit unique variability in HoxD11 transcription factor binding sites. These may influence the spatiotemporal position of their lumbosacral transition.