Among fungi, the basic life strategies are saprophytism, parasitism, and predation. Fungi in Orbiliaceae (Ascomycota) prey on animals by means of specialized trapping structures. Five types of trapping devices are recognized, but their evolutionary origins and divergence are not well understood. Based on comprehensive phylogenetic analysis of nucleotide sequences of three protein-coding genes (RNA polymerase II subunit gene, rpb2; elongation factor 1-␣ gene, ef1-␣; and ß tubulin gene, bt) and ribosomal DNA in the internal transcribed spacer region, we have demonstrated that the initial trapping structure evolved along two lineages yielding two distinct trapping mechanisms: one developed into constricting rings and the other developed into adhesive traps. Among adhesive trapping devices, the adhesive network separated from the others early and evolved at a steady and gentle speed. The adhesive knob evolved through stalk elongation, with a final development of nonconstricting rings. Our data suggest that the derived adhesive traps are at a highly differentiated stage. The development of trapping devices is felicitous proof of adaptive evolution.

For decades, essential hypertension has been primarily viewed from a hemodynamic, neural, and renal perspective. However, based on mounting evidence from clinical, epidemiological, and experimental studies, it has become increasingly recognized that disturbances in carbohydrate and lipid metabolism often accompany high blood pressure, and that essential hypertension may also represent a disorder of cardiovascular endocrinology and metabolism (1, 2). In patients with essential hypertension, clustering of metabolic cardiovascular risk factors -including glucose intolerance, hyperinsulinemia, and hypertriglyceridemiamay promote susceptibility to target organ damage and partly explain why conventional antihypertensive agents have failed to reduce the risk for coronary heart disease to the extent predicted from epidemiological studies (2).Recently, a provocative hypothesis has emerged in which inherited disorders of carbohydrate or lipid metabolism are held to be at the core of the hypertension syndrome and to contribute to the primary pathogenesis of increased blood pressure. Studies in nonobese subjects with a family history of hypertension and in a variety of experimental animal models have suggested that alterations in carbohydrate and/or lipid metabolism can influence the regulation of blood pressure and might precede the development of hypertension (3-5). The lack of insulin resistance in patients with secondary forms of hypertension, together with observations of disordered carbohydrate and lipid metabolism in cultured adipocytes from hypertensive animals, indicates that at least some endocrine-metabolic disturbances are not simply a consequence of increased blood pressure (4,(6)(7)(8). Hence, there is intense interest in identifying genetic mechanisms that may underlie the association between increased blood pressure and other cardiovascular risk factors in essential hypertension.The spontaneously hypertensive rat (SHR) is the most Disorders of carbohydrate and lipid metabolism have been reported to cluster in patients with essential hypertension and in spontaneously hypertensive rats (SHRs). A deletion in the Cd36 gene on chromosome 4 has recently been implicated in defective carbohydrate and lipid metabolism in isolated adipocytes from SHRs. However, the role of Cd36 and chromosome 4 in the control of blood pressure and systemic cardiovascular risk factors in SHRs is unknown. In the SHR.BN-Il6/Npy congenic strain, we have found that transfer of a segment of chromosome 4 (including Cd36) from the Brown Norway (BN) rat onto the SHR background induces reductions in blood pressure and ameliorates dietary-induced glucose intolerance, hyperinsulinemia, and hypertriglyceridemia. These results demonstrate that a single chromosome region can influence a broad spectrum of cardiovascular risk factors involved in the hypertension metabolic syndrome. However, analysis of Cd36 genotypes in the SHR and stroke-prone SHR strains indicates that the deletion variant of Cd36 was not critical to the initial selection for hypert...

Carnivorism is one of the basic life strategies of fungi. Carnivorous fungi possess the ability to trap and digest their preys by sophisticated trapping devices. However, the origin and development of fungal carnivorism remains a gap in evolution biology. In this study, five protein-encoding genes were used to construct the phylogeny of the carnivorous fungi in the phylum Ascomycota; these fungi prey on nematodes by means of specialized trapping structures such as constricting rings and adhesive traps. Our analysis revealed a definitive pattern of evolutionary development for these trapping structures. Molecular clock calibration based on two fossil records revealed that fungal carnivorism diverged from saprophytism about 419 Mya, which was after the origin of nematodes about 550–600 Mya. Active carnivorism (fungi with constricting rings) and passive carnivorism (fungi with adhesive traps) diverged from each other around 246 Mya, shortly after the occurrence of the Permian–Triassic extinction event about 251.4 Mya. The major adhesive traps evolved around 198–208 Mya, which was within the time frame of the Triassic–Jurassic extinction event about 201.4 Mya. However, no major carnivorous ascomycetes divergence was correlated to the Cretaceous–Tertiary extinction event, which occurred more recently (about 65.5 Mya). Therefore, a causal relationship between mass extinction events and fungal carnivorism evolution is not validated in this study. More evidence including additional fossil records is needed to establish if fungal carnivorism evolution was a response to mass extinction events.