As climate change progresses, we are observing widespread changes in phenotypes in many plant populations. Whether these phenotypic changes are directly caused by climate change, and whether they result from phenotypic plasticity or evolution, are active areas of investigation. Here, we review terrestrial plant studies addressing these questions. Plastic and evolutionary responses to climate change are clearly occurring. Of the 38 studies that met our criteria for inclusion, all found plastic or evolutionary responses, with 26 studies showing both. These responses, however, may be insufficient to keep pace with climate change, as indicated by eight of 12 studies that examined this directly. There is also mixed evidence for whether evolutionary responses are adaptive, and whether they are directly caused by contemporary climatic changes. We discuss factors that will likely influence the extent of plastic and evolutionary responses, including patterns of environmental changes, species’ life history characteristics including generation time and breeding system, and degree and direction of gene flow. Future studies with standardized methodologies, especially those that use direct approaches assessing responses to climate change over time, and sharing of data through public databases, will facilitate better predictions of the capacity for plant populations to respond to rapid climate change.

The organization of the inferior pulvinar complex (PI) in squirrel monkeys was studied with histochemical localization of the calcium binding proteins calbindin-D28k and parvalbumin, and of cytochrome oxidase. With each of these markers, the inferior pulvinar complex can be subdivided into four distinct regions. Calbindin-D28k immunoreactivity is densely distributed in cells and neuropil within PI, except for a distinct centromedially located gap. This calbindin-poor zone, termed the medial division of the inferior pulvinar (PIM), corresponds precisely to a region that contains elevated cytochrome oxidase activity and parvalbumin immunostaining. The PIM extends slightly above and behind the classically defined limit of the inferior pulvinar, the corticotectal tract. Regions of inferior pulvinar with intense immunostaining for calbindin-D28k were the posterior division of the inferior pulvinar (PIP, medial to PIM) and the central division (PIC, lateral to PIM). A newly recognized lateral region, PIL, adjoins the lateral geniculate nucleus and stains more lightly for calbindin and parvalbumin immunoreactivity and for cytochrome oxidase. Staining patterns for calbindin, parvalbumin, and cytochrome oxidase in the pulvinar of rhesus monkeys closely resemble those shown in squirrel monkey inferior pulvinar, suggesting that a common organization exists in all primates. In order to examine cortical connection patterns of the histochemically defined compartments in the inferior pulvinar, injections of up to five neuroanatomical tracers (wheat germ agglutinin conjugated to horseradish peroxidase and fluorescent retrograde tracers) were placed in the same cerebral hemisphere. Single injection sites were in the middle temporal area (MT), and several separate injections were placed in a strip corresponding to the rostral subdivision of the dorsolateral area (DLr). Injections that involved only DLr and not MT labeled principally the PIC, and more sparsely PIP and PIL. DLr connections occupied a "shell" region dorsal to PIM that extended from PIC into the lateral and medial divisions of the pulvinar, PL and PM. Injection sites that included MT or were largely restricted to MT produced dense label in PIM and moderate label in PIC and PIL. The retinotopic organization within the inferior pulvinar was inferred from patterns of connections. Connections with cortex related most closely to central vision were found posteriorly in PIM and in adjacent portions of PIC as it wraps around the caudal pole of PIM. Cortex related to more peripheral locations in the lower visual field connected with more rostral PIM and PIC. Patterns of label within the portions of PL and PM that were immediately adjacent to PIM roughly paralleled those in PIM and PIC.(ABSTRACT TRUNCATED AT 400 WORDS)

Autoradiographic tracing procedures have been used to study the organization of retinogeniculate axons in seven primates, i.e., four species of New World monkeys, one species of Old World monkeys and two species of prosimians. These data suggest that the basic primate pattern of geniculate lamination consists of two parvocellular layers, two magnocellular layers, and two poorly developed and highly variable superficial (S) layers which are ventrally located. Ocular input to each member of each of the three pairs differs. In the macaque, the squirrel, and the saki monkey, the parvocellular layers subdivide and interdigitate into four leaflets so as to give the appearance of four parvocellular "layers." These leaflets are much less extensive in the owl and marmoset monkeys. In some individual macaque monkeys, there is further splitting of the parvocellular leaflets into subleaflets, giving the appearance of six parvocellular "layers." The prosimians (galago and slow loris) have two additional layers that are not found in pithecoid primates, and only one superficial layer is apparent. The two additional layers are termed "koniocellular" since they consist of very small cells. Finally, New and Old World monkeys have both ipsilateral and contralateral retinal input to the interlaminar zones. We conclude that the basic pattern of lateral geniculate organization is six layers, but not the traditional six. Prosimians have evolved two additional layers, the koniocellular layers, and have possibly lost one superficial layer. Both New World and Old World monkeys have elaborated the parvocellular layers by forming leaflets to varying extents. With the possible exception of the single S layer in prosimians, layers form pairs that are similar in cell types, but different in ocular input.

Background Bronchiolitis obliterans syndrome (BOS) is a major cause of morbidity and mortality post lung transplantation (LTx). We sought to determine the relationship between alloimmune responses and autoimmunity, and subsequently how autoimmunity leads to chronic rejection. Methods We analyzed the development of donor specific antibodies (Abs) in LTx by flow PRA and the development of Abs to K-α1 tubulin (K-α1T) and collagen V (ColV) by ELISA. The frequency of K-α1T and ColV specific T cells that secrete IFN-γ, IL-17 and IL-10 in LTx recipients was measured by ELSIPOT. Results In a retrospective analysis of 42 LTx recipients, we demonstrated a strong correlation between development of donor specific anti-HLA Abs, Abs to self-antigens, and BOS (p<0.05). To test the hypothesis that alloimmunity is related to an immune response to self-antigens, we analyzed 103 LTx patients prospectively for the development of donor specific Abs (DSA) and Abs to self-antigens. 42.7% of recipients developed DSA and 30.1% developed Abs to K-α1T and ColV. Development of DSA preceded development of Abs to self-antigens. BOS+ patients had higher frequency of T-cells secreting IL-17 (p<0.01) and IFNγ (p<0.05) with decreased IL-10 (p<0.05) compared to BOS- patients. Conclusion Based on these results we propose that alloimmune responses to donor HLA can induce autoimmune responses to airway epithelial self-antigens, characterized by activation of the IL-17 pathway. These immune responses to self-antigens along with alloimmunity contribute to the pathogenesis of BOS. Strategies to prevent development of autoimmunity may be important in preventing the development of chronic rejection.

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