Equine half sibs with an unbalanced X;15 translocation or trisomy 28

Two unrelated chromosome abnormalities were found in equine half sibs. The proposita, Case 1, which was short in stature and infertile, had a de novo unbalanced X;15 translocation involving loss of Xp. Replication studies indicated that the translocated X was preferentially late replicating and that this late replication spread variably into the autosomal segment. Case 2, a half brother of the proposita, was short in stature, had cryptorchidism, and was trisomic for chromosome 28. Cytogenetic analysis of the dam, the sire of Case 1, and two other phenotypically normal half sibs revealed normal chromosome complements. Five further normal pregnancies were reported. The finding of two unrelated chromosome abnormalities is therefore probably fortuitous in this family. This is the first case of an unbalanced X-autosome translocation and the first case of an autosome trisomy to be reported in the horse.     

A neuronal inhibitory domain in the N‐terminal half of agrin

Agrin is required for appropriate pre‐ and postsynaptic differentiation of neuromuscular junctions. While agrin's ability to orchestrate postsynaptic differentiation is well documented, more recent experiments have suggested that agrin is also a “stop signal” for the presynaptic neuron, and that agrin has actions on neurons in the CNS. To elucidate the neuronal activities of agrin and to define the receptor(s) responsible for these functions, we have examined adhesions of neurons and their neurite‐outgrowth responses to purified agrin in vitro. We find that both full‐length agrin and the C‐terminal 95 kDa of agrin (agrin c95), which is sufficient to induce postsynaptic differentiation, are adhesive for chick ciliary ganglion (CG) and forebrain neurons. Consistent with previous findings, our results show that N‐CAM binds to full‐length agrin, and suggest that α‐dystroglycan is a neuronal receptor for agrin c95. In neurite outgrowth assays, full‐length agrin inhibited both laminin‐ and N‐cadherin–induced neurite growth from CG neurons. The N‐terminal 150 kDa fragment of agrin, but not agrin c95, inhibited neurite outgrowth, indicating that domains in the N‐terminal portion of agrin are sufficient for this function. Adhesion assays using protein‐coated beads and agrin‐expressing cells revealed differential interactions of agrin with members of the immunoglobulin superfamily of cell adhesion molecules. However, none of these, including N‐CAM, appeared to be critical for neuronal adhesion. In summary, our results suggest that the N‐terminal half of agrin is involved in agrin's ability to inhibit neurite outgrowth. Our results further suggest that neither α‐dystroglycan nor N‐CAM, two known binding proteins for agrin, mediate this effect. © 2002 Wiley Periodicals, Inc. J Neurobiol 50: 164–179, 2002; DOI 10.1002/neu.10025     

Learning with half a brain

Since the 1970s, human subjects that have undergone corpus callosotomy have provided important insights into neural mechanisms of perception, memory, and cognition. The ability to test the function of each hemisphere independently of the other offers unique advantages for investigating systems that are thought to underlie cognition. However, such approaches have been limited to mammals. Here we describe comparable experiments on an insect brain to demonstrate learning‐associated changes within one brain hemisphere. After training one half of their bisected brains, cockroaches learn to extend the antenna supplying that brain hemisphere towards an illuminated diode after this has been paired with an odor stimulus. The antenna supplying the naïve hemisphere shows no response. Cockroaches retain this ability for up to 24 h, during which, shortly after training, the mushroom body of the trained hemisphere alone undergoes specific post‐translational alterations of microglomerular synaptic complexes in its calyces. © 2007 Wiley Periodicals, Inc. Develop Neurobiol, 2007.     

Spherosome membranes: half unit-membranes

Spherosomes are bounded by unusual single-line “membranes” which measure 2 to 3.5 nanometers in width, contrasted to the well known tripartite unit-membranes which measure 6 to 8.5 nanometers in over-all thickness. Juxtaposed externally (from the side addressing the hyaloplasm), two spherosomal membranes adjoin to form a thicker single line, but apposed internally (the sides that contact stored lipid) two single-line membranes touch to form a tripartite structure resembling a unit-membrane. Morphologically, we interpret the single-line membranes of spherosomes as half unit-membranes whose polar surfaces face the hyaloplasm and whose lipoidal nonpolar surfaces contact internal storage lipid.     

Impacts of a half century of sea‐level rise and development on an endangered mammal

The extraordinary growth of human populations and development in coastal areas over the last half century has eliminated and degraded coastal habitats and threatened the persistence of associated wildlife. Moreover, human‐induced sea‐level rise (SLR) is projected to further eliminate and alter the same coastal ecosystems, especially low‐lying regions. Whereas habitat loss and wildlife population declines from development are well documented, contemporary SLR has not yet been implicated in declines of coastal faunal populations. In addition, the projection of severe synergistic impacts from the combination of development and SLR is well described, yet the scientific literature offers little empirical evidence of the influence of these forces on coastal wildlife. Analysis of aerial photographs from 1959 to 2006 provided evidence of a 64% net loss of the endangered Lower Keys marsh rabbit's (Sylvilagus palustris hefneri; LKMR) habitat, the majority due to SLR (>48%). Furthermore, there was a strong negative relationship between the proportion of development per island and the amount of new habitat formed. Islands with modest development (less than 8% of land area) saw formation of new areas of marsh vegetation suitable for rabbits, whereas islands with 8% or more of their lands developed between 1959 and 2006 saw little to no addition of LKMR habitat. Only 8% of habitat loss was directly due to conversion to impervious surfaces, indicating that the greatest threats from development were indirect, including blocking of the inland migration of habitat triggered by SLR. Our results were consistent with an ongoing squeeze of coastal ecosystems between rising seas and development as a threat to LKMR habitat, which raises concern for a wide variety of coastal species. Our results provide evidence that SLR has become a contemporary conservation concern, one that is exacerbated by development, and expected to increase in magnitude as ocean waters continue to rise.     

Four and a half LIM domain protein signaling and cardiomyopathy

Four and a half LIM domain (FHL) protein family members, FHL1 and FHL2, are multifunctional proteins that are enriched in cardiac muscle. Although they both localize within the cardiomyocyte sarcomere (titin N2B), they have been shown to have important yet unique functions within the context of cardiac hypertrophy and disease. Studies in FHL1-deficient mice have primarily uncovered mitogen-activated protein kinase (MAPK) scaffolding functions for FHL1 as part of a novel biomechanical stretch sensor within the cardiomyocyte sarcomere, which acts as a positive regulator of pressure overload-mediated cardiac hypertrophy. New data have highlighted a novel role for the serine/threonine protein phosphatase (PP5) as a deactivator of the FHL1-based biomechanical stretch sensor, which has implications in not only cardiac hypertrophy but also heart failure. In contrast, studies in FHL2-deficient mice have primarily uncovered an opposing role for FHL2 as a negative regulator of adrenergic-mediated signaling and cardiac hypertrophy, further suggesting unique functions targeted by FHL proteins in the “stressed” cardiomyocyte. In this review, we provide current knowledge of the role of FHL1 and FHL2 in cardiac muscle as it relates to their actions in cardiac hypertrophy and cardiomyopathy. A specific focus will be to dissect the pathways and protein-protein interactions that underlie FHLs’ signaling role in cardiac hypertrophy as well as provide a comprehensive list of FHL mutations linked to cardiac disease, using evidence gained from genetic mouse models and human genetic studies.     

<Emphasis Type="Italic">In vitro</Emphasis> phosphorylation of the N-terminal half of hordeivirus movement protein

The N-terminal half of TGB1 movement protein of poa semilatent hordeivirus, which forms a ribonucleoprotein complex involved in movement of the viral genome in the plant, and its two domains, NTD and ID, are phosphorylated in vitro by a fraction enriched in cell walls from Nicotiana benthamiana. Using a set of protein kinase inhibitors with different specificities, it was found that enzymes possessing activities of casein kinase 1, protein kinase A, and protein kinase C are involved in phosphorylation. Commercial preparations of protein kinases A and C are able to phosphorylate in vitro recombinant proteins corresponding to the N-terminal half of the protein and its domains NTD and ID. Phosphorylation of the NTD has no effect on the efficiency and character of its binding to RNA. However, phosphorylation of the ID leads to a decrease in its RNA-binding activity and in the ability for homological protein-protein interactions.