Diseases of wild and cultured juvenile crustaceans: Insights from below the minimum landing size

Decapod crustaceans (i.e., lobsters, crabs, and shrimps) are all subject to disease, both in the wild and in culture. No life stage appears to be immune to some form of pathogen or parasite. However, juveniles appear to be the targets of some of the most pervasive and consequential diseases. It is therefore surprising, given the enormous economic value of adult decapods, that we know so little about the effects of pathogens on their vulnerable life stage. Here I review the significant diseases reported for juvenile decapods that support fisheries and aquaculture, and highlight research that demonstrates the advantage of incorporating juveniles and ecology in studies of disease.     

Expression, purification and structural analysis of the Pyrococcus abyssi RNA binding protein PAB1135

Background

Epistatic interactions of multiple single nucleotide polymorphisms (SNPs) are now believed to affect individual susceptibility to common diseases. The detection of such interactions, however, is a challenging task in large scale association studies. Ant colony optimization (ACO) algorithms have been shown to be useful in detecting epistatic interactions.

Findings

AntEpiSeeker, a new two-stage ant colony optimization algorithm, has been developed for detecting epistasis in a case-control design. Based on some practical epistatic models, AntEpiSeeker has performed very well.

Conclusions

AntEpiSeeker is a powerful and efficient tool for large-scale association studies and can be downloaded from http://nce.ads.uga.edu/~romdhane/AntEpiSeeker/index.html.     

A morphological and immunohistochemical comparison of mammary tissues from the short-tailed fruit bat (Carollia perspicillata) and the mouse

In the present study, mammary tissues from the fruit bat (Carollia perspicillata) and mouse (Mus musculus) were compared using histological and immunohistochemical methods. Because the female bat exhibits greater reproductive similarities to humans, it might provide a useful animal model for studying mammary physiology and disease with relevance to our own species. In lactating and recently lactating specimens, bat tissue had significantly fewer adipocytes and more collagenous connective tissue compared to the mouse. The proteins Stat5a, keratin 5, Npt2b, and E-cadherin were all similarly localized in mouse and bat mammary tissues taken from lactating animals. The present study demonstrates that whereas the epithelial compartment and the presence of differentiation markers are conserved between the mouse and bat, differences exist in the stromal compartment.     

Angiomotin regulates visceral endoderm movements during mouse embryogenesis

In pregastrula stage mouse embryos, visceral endoderm (VE) migrates from a distal to anterior position to initiate anterior identity in the adjacent epiblast. This anterior visceral endoderm (AVE) is then displaced away from the epiblast by the definitive endoderm to become associated with the extra-embryonic ectoderm and subsequently contributes to the yolk sac. Little is known about the molecules that regulate this proximal displacement. Here we describe a role for mouse angiomotin (amot) in VE movements. amot expression is initially detected in the AVE and subsequently in the VE associated with the extra-embryonic ectoderm. Most amot mutant mice die soon after gastrulation with distinct furrows of VE located at the junction of the embryonic and extra-embryonic regions. Mutant analysis suggests that VE accumulation in these furrows is caused by defects in cell migration into proximal extra-embryonic regions, although distal-to-anterior movements associated with the epiblast, definitive endoderm formation, and anterior specification of the epiblast appear to be normal. These results suggest that amot acts within subregions of the VE to regulate morphogenetic movements that are required for embryo viability.     

The allocation and differentiation of mouse primordial germ cells.

Analysis of the lineage potency of epiblast cells of the early-streak stage mouse embryo reveals that the developmental fate of the cells is determined by their position in the germ layer. Epiblast cells that are fated to become neuroectoderm can give rise to primordial germ cells (PGCs) and other types of somatic cells when they were transplanted to the proximal region of the epiblast. On the contrary, proximal epiblast cells transplanted to the distal region of the embryo do not form PGCs. Therefore, the germ line in the mouse is unlikely to be derived from a predetermined progenitor population, but may be specified as a result of tissue interactions that take place in the proximal epiblast of the mouse gastrula. The initial phase of the establishment of the PGC population requires, in addition to BMP activity emanating from the extraembryonic ectoderm, normal Lim1 and Hnf3beta activity in the germ layers. The entire PGC population is derived from a finite number of progenitor cells and there is no further cellular recruitment to the germ line after gastrulation. The XX PGCs undergo X-inactivation at the onset of migration from the gut endoderm and re-activate the silenced X-chromosome when they enter the urogenital ridge. Germ cells that are localised ectopically in extragonadal sites do not re-activate the X-chromosome, even when nearly all germ cells in the fetal ovary have restored full activity of both X-chromosomes. XXSxr germ cells can re-activate the X-chromosome in the sex-reversed testis, suggesting that the regulation of X-chromosome activity is independent of ovarian morphogenesis.     

The early time course of the inhibition of stem growth of etiolated pea seedlings by fluorescent light

The stem elongation responses of etiolated peas (Pisum sativum L.) to fluorescent light (35–45 mol.m^t-2.s^-1) were recorded using high resolution position transducers. Continuous fluorescent light decreased growth by 70% within 9 min. The growth rate declined to 5% of the control over the next 2 h and remained at this level for 7 h. Pulses of fluorescent light ranging from 8 s to 34 min led to partial suppression of growth and resulted in a complex kinetic response. The distinctive kinetics of blue and red light inhibition were apparent as components of the responses to non-saturating levels of fluorescent light. The rapid suppression of growth by blue light was not affected by concomitant red light. The lag time for the onset of red light inhibition was not affected by concomitant blue, but the rate of inhibition appeared accelerated.     

Protease activity associated with loss of adhesiveness in mouse teratocarcinoma

Actin-binding proteins were assayed in various tissues using an 125I-actin overlay procedure. Four major G actin-binding proteins of 90000, 65000, 58000 and 40000 Mr have been identified. The 90K protein is present in all tissues and binds labelled actin in a calcium-sensitive manner with binding increasing 3-4-fold in the presence of Ca2+. The distribution of the 58K and 65K protein which are not Ca2+-sensitive was more variable. These proteins were present in different ratios in different tissues. 125I-actin binding to all four actin-binding proteins is specific and can be displaced by preincubation of the gels with unlabelled actin. The interaction of actin with these proteins does not appear to involve ionic forces, since binding is not diminished by varying the salt concentration. Skeletal muscle glycolytic enzymes, the lens crystallins and the histones also bind 125I-actin. This binding cannot be displaced by preincubation with unlabelled actin and is presumably non-specific. The calcium sensitivity of two highly purified actin-binding proteins, the 90K human platelet protein and villin was compared using 125I-actin. The platelet 90K protein binds actin at less than 10(-7) M free calcium, but detectable binding to villin does not occur below 10(-6) M free calcium. The ubiquity of these actin-binding proteins is clear and we conclude that the calcium-sensitive 90K actin-binding protein in all of these tissues is the same as the platelet protein.     

Ethylene plays multiple nonprimary roles in modulating the gravitropic response in tomato.

Ethylene is known to interact with auxin in regulating stem growth, and yet evidence for the role of ethylene in tropic responses is contradictory. Our analysis of four mutants of tomato (Lycopersicon esculentum) altered in their response to gravity, auxin, and/or ethylene revealed concentration-dependent modulation of shoot gravitropism by ethylene. Ethylene inhibitors reduce wild-type gravicurvature, and extremely low (0.0005-0.001 microliter L-1) ethylene concentrations can restore the reduced gravitropic response of the auxin-resistant dgt (diageotropica) mutant to wild-type levels. Slightly higher concentrations of ethylene inhibit the gravitropic response of all but the ethylene-insensitive nr (never-ripe) mutant. The gravitropic responses of nr and the constitutive-response mutant epi (epinastic) are slightly and significantly delayed, respectively, but otherwise normal. The reversal of shoot gravicurvature by red light in the lz-2 (lazy-2) mutant is not affected by ethylene. Taken together, these data indicate that, although ethylene does not play a primary role in the gravitropic response of tomato, low levels of ethylene are necessary for a full gravitropic response, and moderate levels of the hormone specifically inhibit gravicurvature in a manner different from ethylene inhibition of overall growth.