remain unaffected. Intermittent feeding also represents a temporal increase in food intake and can induce dramatic changes in the size of the gut; the Burmese python (Python molurus bivittatus) can triple the size of its small intestine just a few days after feeding. AMY2B (Alpha-Amylase 2B) is a gene that codes a protein that assists with the first step in the digestion of dietary starch and glycogen. An expansion of this gene in dogs would enable early dogs to exploit a starch-rich diet as they fed on refuse from agriculture. Data indicated that the wolves and dingo had just two copies of the gene and the Siberian Husky that is associated with hunter-gatherers had just three or four copies, whereas the Saluki that is associated with the Fertile Crescent where agriculture originated had 29 copies. The results show that on average, modern dogs have a high copy number of the gene, whereas wolves and dingoes do not. The high copy number of AMY2B variants likely already existed as a standing variation in early domestic dogs, but expanded more recently with the development of large agriculturally based civilizations. Parasitism Infection with parasites can induce phenotypic plasticity as a means to compensate for the detrimental effects caused by parasitism. Commonly, invertebrates respond to parasitic castration or increased parasite virulence with fecundity compensation in order to increase their reproductive output, or fitness. For example, water fleas (Daphnia magna), exposed to microsporidian parasites produce more offspring in the early stages of exposure to compensate for future loss of reproductive success. A reduction in fecundity may also occur as a means of re-directing nutrients to an immune response, or to increase longevity of the host. This particular form of plasticity has been shown in certain cases to be mediated by host-derived molecules (e.g. schistosomin in snails Lymnaea stagnalis infected with trematodes Trichobilharzia ocellata) that interfere with the action of reproductive hormones on their target organs. Changes in reproductive effort during infection is also thought to be a less costly alternative to mounting resistance or defence against invading parasites, although it can occur in concert with a defence response. Hosts can also respond to parasitism through plasticity in physiology aside from reproduction. House mice infected with intestinal nematodes experience decreased rates of glucose transport in the intestine. To compensate for this, mice increase the total mass of mucosal cells, cells responsible for glucose transport, in the