Fossil evidence for a pharyngeal origin of the vertebrate pectoral girdle

The origin of vertebrate paired appendages is one of the most investigated and debated examples of evolutionary novelty. Paired appendages are widely considered key innovations that allowed new opportunities for controlled swimming and gill ventilation and were prerequisites for the eventual transition from water to land. The last 150 years of debate has been shaped by two contentious theories: the ventrolateral fin-fold hypothesis and the archipterygium hypothesis. The latter proposes that fins and girdles evolved from an ancestral gill arch. Although tantalizing developmental evidence has revived interest in this idea, it is apparently unsupported by fossil evidence. Here we present fossil evidence of a pharyngeal basis for the vertebrate shoulder girdle. We use CT scanning to reveal details of the braincase of Kolymaspis sibirica, a placoderm fish from the Early Devonian of Siberia that suggests a pharyngeal component of the shoulder. We combine these findings with refreshed comparative anatomy of placoderms and jawless outgroups to place the origin of the shoulder girdle on the sixth branchial arch. These findings provide a novel framework for understanding the origin of the pectoral girdle. Our new evidence clarifies the location of the presumptive head-trunk interface in jawless fishes and explains the constraint on branchial arch number in gnathostomes. The results revive a key aspect of the archipterygium hypothesis, but also reconciles it with the ventrolateral fin fold model

Localized Suppression of Inflammation at Sites of Helicobacter pylori Colonization ▿

While gastric adenocarcinoma is the most serious consequence of Helicobacter pylori infection, not all infected persons develop this pathology. Individuals most at risk of this cancer are those in whom the bacteria colonize the acid-secreting region of the stomach and subsequently develop severe inflammation in the gastric corpus. It has been reported anecdotally that male mice become infected with greater numbers of H. pylori bacteria than female mice. While investigating this phenomenon, we found that increased H. pylori infection densities in male mice were not related to antibody production, and this phenomenon was not normalized by gonadectomy. However, the gastric pH in male 129/Sv mice was significantly elevated compared with that in female mice. Differences in colonization were evident within 1 day postinfection and significantly arose due to colonization of the gastric corpus region in male mice. This provided a potential model for comparing the effect of corpus colonization on the development of gastritis. This was explored using two models of H. pylori-induced inflammation, namely, 2-month infections of Muc1−/− mice and 6-month infections of wild-type 129/Sv mice. While H. pylori infection of female mice induced a severe, corpus-predominant atrophic gastritis, to our surprise, male mice developed minimal inflammation despite being colonized with significantly more H. pylori bacteria than female controls. Thus, colonization of the gastric corpus in male mice was associated with a loss of inflammation in that region. The suppression of inflammation concomitant with infection of the gastric corpus in male mice demonstrates a powerful localized suppression of inflammation induced at sites of H. pylori colonization