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Using corridors for conservation is increasing despite a lack of consensus on their efficacy. Specifically, whether corridors increase movement of plants and animals between habitat fragments has been addressed on a case-by-case basis with mixed results. Because of the growing number of well-designed experiments that have addressed this question, we conducted a meta-analysis to determine whether corridors increase movement; whether corridor effectiveness differs among taxa; how recent changes in experimental design have influenced findings; and whether corridor effectiveness differs between manipulative and natural experiments. To conduct our meta-analysis, we analyzed 78 experiments from 35 studies using a conservative hierarchical Bayesian model that accounts for hierarchical and sampling dependence. We found a highly significant result that corridors increase movement between habitat patches by approximately 50% compared to patches that are not connected with corridors. We found that corridors were more important for the movement of invertebrates, nonavian vertebrates, and plants than they were for birds. Recent methodological advances in corridor experiments, such as controlling for the area added by corridors, did not influence whether corridors increased movement, whereas controlling for the distance between source and connected or unconnected recipient patches decreased movement through corridors. After controlling for taxa differences and whether studies controlled for distance in experimental design, we found that natural corridors (those existing in landscapes prior to the study) showed more movement than manipulated corridors (those created and maintained for the study). Our results suggest that existing corridors increase species movement in fragmented landscapes and that efforts spent on maintaining and creating corridors are worthwhile.

PURPOSE: Seizures are noted in a significant proportion of cases of de novo, heterozygous, loss-of-function mutations in SOX2, ascertained because of severe bilateral eye malformations. We wished to determine the underlying cerebral phenotype in SOX2 mutation and to test the candidacy of SOX2 as a gene contributing to human epilepsies. METHODS: We examined high-resolution MRI scans in four patients with SOX2 mutations, two of whom had seizures. We determined the Sox2 expression pattern in developing murine brain. We searched for SOX2 mutation in 24 patients with typical hippocampal sclerosis and for common variations in SOX2 in 655 patients without eye disease but with epilepsy, including 91 patients with febrile seizures, 93 with hippocampal sclerosis, and 258 with temporal lobe epilepsy. RESULTS: Striking hippocampal and parahippocampal malformations were seen in all cases, with a history of febrile seizures or epilepsy in two of four cases. The Sox2 expression pattern in developing mouse brain supports the pattern of malformations observed. Mutation screening in patients with epilepsy did not reveal any abnormalities in SOX2. No associations were found between any clinical epilepsy phenotype and common variation in SOX2. CONCLUSIONS: SOX2 haploinsufficiency causes mesial temporal malformation in humans, making SOX2 dysfunction a candidate mechanism for mesial temporal abnormalities associated with chronic epilepsy. However, although mutation of SOX2 in humans causes hippocampal malformation, SOX2 mutation or variation is unlikely to contribute commonly to mesial temporal lobe epilepsy or its structural (hippocampal sclerosis) or historic (febrile seizures) associations in humans.