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Tardigrades can survive hostile environments such as desiccation by adopting a state of anhydrobiosis. Numerous tardigrade species have been described thus far, and recent genome and transcriptome analyses revealed that several distinct strategies were employed to cope with harsh environments depending on the evolutionary lineages. Detailed analyses at the cellular and subcellular levels are essential to complete these data. In this work, we analyzed a tardigrade species that can withstand rapid dehydration, Ramazzottius varieornatus. Surprisingly, we noted an absence of the anhydrobiotic-specific extracellular structure previously described for the Hypsibius exemplaris species. Both Ramazzottius varieornatus and Hypsibius exemplaris belong to the same evolutionary class of Eutardigrada. Nevertheless, our observations reveal discrepancies in the anhydrobiotic structures correlated with the variation in the anhydrobiotic mechanisms. [ABSTRACT FROM AUTHOR]

The dynamic equilibrium between death and regeneration is well established at the cell level. Conversely, no study has investigated the homeostatic control of shape at the whole organism level through processes involving apoptosis. To address this fundamental biological question, we took advantage of the morphological and functional properties of the carnivorous sponge Lycopodina hypogea. During its feeding cycle, this sponge undergoes spectacular shape changes. Starved animals display many elongated filaments to capture prey. After capture, prey are digested in the absence of any centralized digestive structure. Strikingly, the elongated filaments actively regress and reform to maintain a constant, homeostatically controlled number and size of filaments in resting sponges. This unusual mode of nutrition provides a unique opportunity to better understand the processes involved in cell renewal and regeneration in adult tissues. Throughout these processes, cell proliferation and apoptosis are interconnected key actors. Therefore, L. hypogea is an ideal organism to study how molecular and cellular processes are mechanistically coupled to ensure global shape homeostasis. [ABSTRACT FROM AUTHOR]

Sponges are an ancient basal life form, so understanding their evolution is key to understanding all metazoan evolution. Sponges have very unusual feeding mechanisms, with an intricate network of progressively optimized filtration units: from the simple choanocyte lining of a central cavity, or spongocoel, to more complex chambers and canals. Furthermore, in a single evolutionary event, a group of sponges transitioned to carnivory. This major evolutionary transition involved replacing the filter-feeding apparatus with mobile phagocytic cells that migrate collectively towards the trapped prey. Here, we focus on the diversity and evolution of sponge nutrition systems and the amazing adaptation to carnivory. [ABSTRACT FROM AUTHOR]

Previous studies have addressed why and how mono‐stratified epithelia adopt a polygonal topology. One major additional, and yet unanswered question is how the frequency of different cell shapes is achieved and whether the same distribution applies between non-proliferative and proliferative epithelia. We compared different proliferative and non-proliferative epithelia from a range of organisms as well as Drosophila melanogaster mutants, deficient for apoptosis or hyperproliferative. We show that the distribution of cell shapes in non‐proliferative epithelia (follicular cells of five species of tunicates) is distinctly, and more stringently organized than proliferative ones (cultured epithelial cells and Drosophila melanogaster imaginal discs). The discrepancy is not supported by geometrical constraints (spherical versus flat monolayers), number of cells, or apoptosis events. We have developed a theoretical model of epithelial morphogenesis, based on the physics of divided media, that takes into account biological parameters such as cell‐cell contact adhesions and tensions, cell and tissue growth, and which reproduces the effects of proliferation by increasing the topological heterogeneity observed experimentally. We therefore present a model for the morphogenesis of epithelia where, in a proliferative context, an extended distribution of cell shapes (range of 4 to 10 neighbors per cell) contrasts with the narrower range of 5-7 neighbors per cell that characterizes non proliferative epithelia. [ABSTRACT FROM AUTHOR]

Caspase-6 is an effector caspase that has not been investigated thoroughly despite the fact that Caspase-6 is strongly activated in Alzheimer disease brains. To understand the full physiological impact of Caspase-6 in humans, we investigated Caspase-6 expression. We performed western blot analyses to detect the pro-Caspase-6 and its active p20 subunit in fetal and adult lung, kidney, brain, spleen, muscle, stomach, colon, heart, liver, skin, and adrenals tissues. The levels were semi-quantitated by densitometry. The results show a ubiquitous expression of Caspase-6 in most fetal tissues with the lowest levels in the brain and the highest levels in the gastrointestinal system. Caspase-6 active p20 subunits were only detected in fetal stomach. Immunohistochemical analysis of a human fetal embryo showed active Caspase-6 positive apoptotic cells in the dorsal root ganglion, liver, lung, kidney, ovary, skeletal muscle and the intestine. In the adult tissues, the levels of Caspase-6 were lower than in fetal tissues but remained high in the colon, stomach, lung, kidney and liver. Immunohistological analyses revealed that active Caspase-6 was abundant in goblet cells and epithelial cells sloughing off the intestinal lining of the adult colon. These results suggest that Caspase-6 is likely important in most tissues during early development but is less involved in adult tissues. The low levels of Caspase-6 in fetal and adult brain indicate that increased expression as observed in Alzheimer Disease is a pathological condition. Lastly, the high levels of Caspase-6 in the gastrointestinal system indicate a potential specific function of Caspase-6 in these tissues. [ABSTRACT FROM AUTHOR]

The tumor suppressor Rb (retinoblastoma protein) is known to regulate p53-dependent apoptosis, but the mechanisms involved are unclear. In a rat fibroblast model, we previously observed that caspase inhibition potentiates p53-dependent apoptosis and prevents the Rb cleavage associated with p53 activation. These results suggested that a caspase(s) can antagonize p53-mediated apoptosis via the production of a protective Rb truncated form. Here, we identify caspase-9 as the caspase that interferes, upstream of the mitochondrion, with p53-induced apoptosis in both immortalized and primary fibroblasts. This caspase can be detected as a p38 processed form in living cells, in the absence of apoptosome formation and apoptotic signal. We also provide evidence that the involvement of caspase-9 in a pre-mitochondrial protective pathway results from the previously undescribed cleavage of Rb, at a LExD site, into a p76Rb form, which antagonizes p53-induced apoptosis. These results establish that a truncated form of Rb can display an antiapoptotic activity, rather than just being a by-product of Rb degradation.Oncogene (2005) 24, 3297-3308. doi:10.1038/sj.onc.1208493 Published online 21 February 2005 [ABSTRACT FROM AUTHOR]

The diurnal changes in carbon and nitrogen metabolite concentrations were studied in transgenic tobacco plants (Nicotiana tabacum L. cv. Xanthi) expressing an antisense ferredoxin-dependent glutamate synthase (Fd-GOGAT; EC 1.4.7.1) mRNA. In parallel, enzyme activities, and abundance of the proteins and transcripts involved in ammonia assimilation were monitored during the day/night cycle in both transgenic and untransformed control plants. When the transgenic plants were transferred from non-photorespiratory (high CO2) to photorespiratory conditions (air), photorespiratory NH4+ accumulated in the leaves during the second half of the light period; it decreased progressively through the night until the beginning of the next light period. Glutamine and 2-oxoglutarate (2-OG) also accumulated during the second part of the light period; this was followed by a decrease at the end of the night. A concomitant increase in asparagine was observed during the night, suggesting that this amino acid serves as a temporary storage compound for the partial elimination of excess photorespiratory ammonia. We also observed that the direction of the glutamate reaction varied during the day/night cycle such that a higher ratio of aminating/deaminating activity occurred in the first half of the light period. This was correlated with the decline in NH4+ and 2-OG concentrations. Both of these observations suggest that alternative metabolic pathways may be transiently activated during a day/night cycle in plants with low Fd-GOGAT activity. [Copyright &y& Elsevier]

With the aim to identify events involved in the determination of p53-dependent apoptosis versus growth arrest, we used rat embryo fibroblasts expressing a temperature-sensitive mutant (tsA58) of the SV40 large tumour antigen (LT). Heat-inactivation of LT leads to p53 activation and commitment to a senescent-like state (REtsA15 cell line) or apoptosis (REtsAF cell line). We report that senescence is associated with high levels of the anti-apoptotic Bcl-2 protein and a cell cycle arrest in G1 phase, whereas apoptosis is associated with low levels of Bcl-2 and a cell cycle arrest in G2 phase. Here we show that Bcl-2, which can inhibit apoptosis and proliferation, turns the apoptotic phenotype into a senescent-like phenotype in G2 phase. This result suggests that Bcl-2-dependent inhibition of apoptosis could be crucial for the commitment to replicative senescence, whereas its ability to inhibit G1 progression would not be required. [Copyright &y& Elsevier]