From sensors to spikes: evolving receptive fields to enhance sensorimotor information in a robot-arm

In biological systems, instead of actual encoders at different joints, proprioception signals are acquired through distributed receptive fields. In robotics, a single and accurate sensor output per link (encoder) is commonly used to track the position and the velocity. Interfacing bio-inspired control systems with spiking neural networks emulating the cerebellum with conventional robots is not a straight forward task. Therefore, it is necessary to adapt this one-dimensional measure (encoder output) into a multidimensional space (inputs for a spiking neural network) to connect, for instance, the spiking cerebellar architecture; i.e. a translation from an analog space into a distributed population coding in terms of spikes. This paper analyzes how evolved receptive fields (optimized towards information transmission) can efficiently generate a sensorimotor representation that facilitates its discrimination from other "sensorimotor states". This can be seen as an abstraction of the Cuneate Nucleus (CN) functionality in a robot-arm scenario. We model the CN as a spiking neuron population coding in time according to the response of mechanoreceptors during a multi-joint movement in a robot joint space. An encoding scheme that takes into account the relative spiking time of the signals propagating from peripheral nerve fibers to second-order somatosensory neurons is proposed. Due to the enormous number of possible encodings, we have applied an evolutionary algorithm to evolve the sensory receptive field representation from random to optimized encoding. Following the nature-inspired analogy, evolved configurations have shown to outperform simple hand-tuned configurations and other homogenized configurations based on the solution provided by the optimization engine (evolutionary algorithm). We have used artificial evolutionary engines as the optimization tool to circumvent nonlinearity responses in receptive fields.     

A barley (Hordeum vulgare L.) LEA3 protein, HVA1, is abundant in protein storage vacuoles

The HVA1 protein belongs to the LEA3 group, which is expressed during the late stage of seed maturation. It is also induced by exogenous abscisic acid (ABA) and a variety of environmental stresses in germinating barley (Hordeum vulgare L.). In the present work, the potential role of HVA1 was investigated by studying its tissue distribution and subcellular localization in mature and stressed seeds by immuno-microscopic methods. In the mature seed, HVA1 protein was detected in all tissues except the non-living starchy endosperm. During germination the amount of HVA1 protein decreased but did not totally disappear. Incubation with 100 μM ABA, cold treatment or drought stress dramatically increased HVA1 expression in the germinated seed. In this work, the distribution of a LEA3 group protein was studied in a cereal seed for the first time by immuno-electron microscopy. In the scutellum and aleurone layer, HVA1 was localized both in the cytoplasm and protein storage vacuoles (PSVs). HVA1 protein was found to be threefold more abundant in PSVs than in the cytoplasm of an unstressed seed tissue. The ratio increased with ABA or stress treatments to at least ninefold. The role of HVA1 in PSVs remains unclear: a previously suggested possibility is ion sequestration to prevent precipitation during stress. On the other hand, HVA1 protein could also be degraded in PSVs. HVA1 protein does not have the signal peptide typical of proteins which are glycosylated and targeted into the vacuole via the Golgi complex. Because HVA1 is not glycosylated, it may use an alternative, ER-independent vacuolar pathway, also found in yeast cells.     

High-Yield Production of a Bacterial Xylanase in the Filamentous Fungus Trichoderma reesei Requires a Carrier Polypeptide with an Intact Domain Structure

A bacterial xylanase gene, Nonomuraea flexuosa xyn11A, was expressed in the filamentous fungus Trichoderma reesei from the strong cellobiohydrolase 1 promoter as fusions to a variety of carrier polypeptides. By using single-copy isogenic transformants, it was shown that production of this xylanase was clearly increased (up to 820 mg/liter) when it was produced as a fusion protein with a carrier polypeptide having an intact domain structure compared to the production (150 to 300 mg/liter) of fusions to the signal sequence alone or to carriers having incomplete domain structures. The carriers tested were the T. reesei mannanase I (Man5A, or MANI) core-hinge and a fragment thereof and the cellulose binding domain of T. reesei cellobiohydrolase II (Cel6A, or CBHII) with and without the hinge region(s) and a fragment thereof. The flexible hinge region was shown to have a positive effect on both the production of Xyn11A and the efficiency of cleavage of the fusion polypeptide. The recombinant Xyn11A produced had properties similar to those of the native xylanase. It constituted 6 to 10% of the total proteins secreted by the transformants. About three times more of the Man5A core-hinge carrier polypeptide than of the recombinant Xyn11A was observed. Even in the best Xyn11A producers, the levels of the fusion mRNAs were only ~10% of the level of cel7A (cbh1) mRNA in the untransformed host strain.     

Sumo-1 function is dispensable in normal mouse development

To elucidate SUMO-1 functions in vivo, we targeted by homologous recombination the last three exons of the murine Sumo-1 gene. Sumo-1 mRNA abundance was reduced to one-half in heterozygotes and was undetectable in Sumo-1(-/-) mice, and SUMO-1-conjugated RanGAP1 was detectable in wild-type mouse embryo fibroblasts (MEFs) but not in Sumo-1(-/-) MEFs, indicating that gene targeting yielded Sumo-1-null mice. Sumo-1 mRNA is expressed in all tissues of wild-type mice, and its abundance is highest in the testis, brain, lungs, and spleen. Sumo-2 and Sumo-3 mRNAs are also expressed in all tissues, but their abundance was not upregulated in Sumo-1-null mice. The development and function of testis are normal in the absence of Sumo-1, and Sumo-1(-)(/)(-) mice of both sexes are viable and fertile. In contrast to a previous report (F. S. Alkuraya et al., Science 313:1751, 2006), we did not observe embryonic or early postnatal demise of Sumo-1-targeted mice; genotypes of embryos and 21-day-old mice were of predicted Mendelian ratios, and there was no defect in lip and palate development in Sumo-1(+/-) or Sumo-1(-/-) embryos. The ability of Sumo-1(-/-) MEFs to differentiate into adipocyte was not different from that of wild-type MEFs. Collectively, our results support the notion that most, if not all, SUMO-1 functions are compensated for in vivo by SUMO-2 and SUMO-3.     

The Effects of Increasing UV-B Radiation on Pigmentation, Growth and Survival of Coregonid Embryos and Larvae

In the northern regions UV-B radiation levels have increased due to ozone depletion. A two-week laboratory experiment was conducted to measure the effects of UV-B radiation on the pigmentation, growth, oxygen consumption rate and survival of whitefish, Coregonus lavaretus, and vendace, Coregonus albula, larvae. In May newly hatched embryos were exposed in laboratory aquaria to three CIE weighted UV-B radiation levels: subambient (daily dose 1.37kJm^–2), 9% (1.81kJm^–2) and 34% higher (2.24kJm^–2) than ambient. Control embryos and larvae were not exposed to UV-B. Larvae of whitefish and vendace that were irradiated with highest UV-B level had 32% and 31% more melanin than control larvae, respectively, which we interpret as an apparent induced response. In controls, the species difference revealed 53% more melanin in vendace larvae than in whitefish larvae. UV-B radiation had no effect on the mortality of either species, the survival being high in all treatments (>90%). Additionally, neither growth rate nor the metabolic rate of larvae of either species was affected by UV-B radiation. Thus, in relation to future scenarios UV-B radiation may not be a threat to whitefish or vendace larvae in current or expected radiation levels.     

Maturation of barley cysteine endopeptidase expressed in Trichoderma reesei is distorted by incomplete processing

Maturation of barley cysteine endopeptidase B (EPB) in Trichoderma reesei was studied with metabolic in hibitors, Western blotting, and immuno microscopy. The inactive 42-kDa recombinant EPB proprotein, first detected in apical cells, was sequentially processed in a time-dependent manner to a secreted polypeptide of 38.5 kDa, and thereafter, to polypeptides of 37.5, 35.5, and 32 kDa exhibiting enzyme activity both in the hyphae and culture medium. The sizes of the different forms of recombinant EPB were in accordance with molecular masses calculated from the deduced amino acid sequence, assuming cleavage at four putative Kex2p sites present in the 42-kDa proprotein. Both the liquid and the zymogram in-gel activity assays indicated that the 32-kDa enzyme produced in T. reesei in vivo was 2 kDa larger and four times less active than the endogenous EPB. Brefeldin A treatment prevented the last Kex2p processing step of EPB from a 35.5- to a 32-kDa protein. This coincided with a significant increase in the immuno-gold label for EPB and in modified Golgi-like bodies, which suggests that the processing step probably took place in medial Golgi. A 30.5-kDa EPB polypeptide was observed when glycosylation was inhibited by tunicamycin (TM) or when deglycosylation was carried out enzymatically. Deglycosylation increased the enzyme activity twofold, which was also indicated by an increased fluorescence by TM treatment in the zymogram in-gel activity assay. Simultaneous incubation with TM and monensin produced a peptide of 31.5 kDa. Therefore, monensin may inhibit the final processing step of an unglycosylated EPB by an unknown protease in the fungus. In any case, the final recombinant EPB product in Trichoderma differs from the mature endogenous 30-kDa enzyme produced in barley.     

Comparing EST-based genetic maps between <Emphasis Type="BoldItalic">Pinus sylvestris</Emphasis> and <Emphasis Type="BoldItalic">Pinus taeda</Emphasis>

A genetic map of Pinus sylvestris was constructed using ESTP (expressed sequence tag polymorphism) markers and other gene-based markers, AFLP markers and microsatellites. Part of the ESTP markers (40) were developed and mapped earlier in Pinus taeda, and additional markers were generated based on P. sylvestris sequences or sequences from other pine species. The mapping in P. sylvestris was based on 94 F₁ progeny from a cross between plus-tree parents E635C and E1101. AFLP framework maps for the parent trees were first constructed. The ESTP and other gene sequence-based markers were added to the framework maps, as well as five published microsatellite loci. The separate maps were then integrated with the aid of AFLPs segregating in both trees (dominant segregation ratios 3:1) as well as gene markers and microsatellites segregating in both parent trees (segregation ratios 1:1:1:1 or 1:2:1). The integrated map consisted of 12 groups corresponding to the P. taeda linkage groups, and additionally three and six smaller groups for E1101 and E635C, respectively. The number of framework AFLP markers in the integrated map is altogether 194 and the number of gene markers 61. The total length of the integrated map was 1,314 cM. The set of markers developed for P. sylvestris was also added to existing maps of two P. taeda pedigrees. Starting with a mapped marker from one pedigree in the source species resulted in a mapped marker in a pedigree of the other species in more than 40% of the cases, with about equal success in both directions. The maps of the two species are largely colinear, even if the species have diverged more than 70 MYA. Most cases of different locations were probably due to problems in identifying the orthologous members of gene families. These data provide a first ESTP-containing map of P. sylvestris, which can also be used for comparing this species to additional species mapped with the same markers.Communicated by C. Möllers