Dither — A Way to reduce undesirable Fright Behavior in ethological Studies1

Wie stark Fluchtstimmung (“Furcht”) das Verhalten von Versuchstieren in ethologischen Untersuchungen stören kann, ist zwar wohl vielen bekannt, wird aber selten erörtert oder in Veröffentlichungen erwähnt. Die Beobachter setzen die Tiere meist entweder der vollen Störung durch den Laborbetrieb aus oder schließen sie weitestgehend von allen möglichen Störreizen ab. Im ersten Fall fehlt die Kontrolle über wichtige Störfaktoren, im zweiten werden vor allem Wirbeltiere oft so furchtsam, daß sie das meiste Verhalten unterdrücken. In Untersuchungen an verschiedenen Fischarten hat sich folgender Ausweg sehr bewährt: Man setzt zum Versuchstier hinter eine durchsichtige Trennwand andersartige Tiere, die sich ständig gleichmäßig bewegen, für das Versuchstier aber ohne Interesse sind.     

Ability of the male recombination factor 31.1 MRF to be transposed to another chromosome in Drosophila melanogaster.

Summary By classical genetic experiments, evidence is provided that the male recombination factor, 31.1 MRF, has the ability to be transposed to another chromosome. The procedure by which the transposition occurs must be different from that of classical crossing over. It appears that transposition occurs only when the factor is active in male germ cells. Moreover, the factor appears to be able to undergo successive transpositions. Furthermore, the integration sites of the factor, when transposed into another chromosome, may not be completely random. Finally, the third chromosome of the 31.1/Cy L ⁴ strain can also induce male recombination.     

Interrelations between the vertical distribution of Daphnia and chlorophyll a in two large limnetic enclosures

This paper summarises the major factors influencing the daytimevertical distribution of Daphnia hyalina var. laciutris (Sars)in two large experimental enclosures (Lund Tubes). In both tubes,the depth at which the Daphnia aggregated during the day wasclosely related to sub-surface ir-radiance. On a few occasionsaggregations of Daphnia were found in ‘dark’ waterassociated with a deep chlorophyll maximum. On many occasions,however, the animals' light response per se ensured their aggregationat depths of maximum phytoplankton abundance. The most importantfactor influencing the dispersion of animals in the water columnwas the steepness of the light gradient. In turbid water verticalaggregations were well defined, whereas in clear water the animalswere widely dispersed around their depth of maximum abundance.Daphnia also tended to disperse in the water column when theirpopulation density was high or when food was scarce. A simplemodel based on surface irradiance, water turbidity and populationdensity explained the basic pattern of vertical distributionthroughout the season. The implications of these findings arediscussed in relation to the effects of zooplankton grazingand speculations on the adaptive significance of depth regulation.     

Organometallic amphiphiles: novel mechanisms for redox chemical control of aggregation behavior

Many natural and synthetic organic amphiphiles have been discovered, prepared, and/or characterized. Aggregation behavior has been studied for many of these monomers. Very few of these many amphiphiles are organometallic compounds and almost nothing is known about this novel group of amphiphiles. Under appropriate circumstances, aggregation of certain organometallic amphiphile monomers can be controlled by use of redox switching. Compounds which are not amphiphilic can be made so and amphiphilic compounds can be deprived of this property by appropriate alterations in the metal ion's oxidation state. Redox-switched aggregation-deaggregation behavior is described for bis(hexadecycloxy)-1,10-phenanthrolinium perchlorate (2), its nickel complex (3), [CH₃(CH₂)₁₅NH₂]₂Ag⁺AcO⁻ (4) and bis(hexadecylamine)copper dichloride (5), chloride acetate (6) and diacetate (7), all of the general formula: [CH₃(CH₂)₁₅NH₂]₂Cu²⁺X₂². Two completely new switching mechanisms are disclosed for the first time which involve electron transfer from dilute aqueous sugar solutions or from solid zinc metal which are effective in collapsing [CH₃(CH₂)₁₅NH₂]₂Cu²⁺X₂²⁻ vesicles.     

SIRT1 Activation by Small Molecules: KINETIC AND BIOPHYSICAL EVIDENCE FOR DIRECT INTERACTION OF ENZYME AND ACTIVATOR?

SIRT1 is a protein deacetylase that has emerged as a therapeutic target for the development of activators to treat diseases of aging. SIRT1-activating compounds (STACs) have been developed that produce biological effects consistent with direct SIRT1 activation. At the molecular level, the mechanism by which STACs activate SIRT1 remains elusive. In the studies reported herein, the mechanism of SIRT1 activation is examined using representative compounds chosen from a collection of STACs. These studies reveal that activation of SIRT1 by STACs is strongly dependent on structural features of the peptide substrate. Significantly, and in contrast to studies reporting that peptides must bear a fluorophore for their deacetylation to be accelerated, we find that some STACs can accelerate the SIRT1-catalyzed deacetylation of specific unlabeled peptides composed only of natural amino acids. These results, together with others of this study, are at odds with a recent claim that complex formation between STACs and fluorophore-labeled peptides plays a role in the activation of SIRT1 (Pacholec, M., Chrunyk, B., Cunningham, D., Flynn, D., Griffith, D., Griffor, M., Loulakis, P., Pabst, B., Qiu, X., Stockman, B., Thanabal, V., Varghese, A., Ward, J., Withka, J., and Ahn, K. (2010) J. Biol. Chem. 285, 8340–8351). Rather, the data suggest that STACs interact directly with SIRT1 and activate SIRT1-catalyzed deacetylation through an allosteric mechanism.     

Ataxin1L Is a Regulator of HSC Function Highlighting the Utility of Cross-Tissue Comparisons for Gene Discovery

Hematopoietic stem cells (HSCs) are rare quiescent cells that continuously replenish the cellular components of the peripheral blood. Observing that the ataxia-associated gene Ataxin-1-like (Atxn1L) was highly expressed in HSCs, we examined its role in HSC function through in vitro and in vivo assays. Mice lacking Atxn1L had greater numbers of HSCs that regenerated the blood more quickly than their wild-type counterparts. Molecular analyses indicated Atxn1L null HSCs had gene expression changes that regulate a program consistent with their higher level of proliferation, suggesting that Atxn1L is a novel regulator of HSC quiescence. To determine if additional brain-associated genes were candidates for hematologic regulation, we examined genes encoding proteins from autism- and ataxia-associated protein–protein interaction networks for their representation in hematopoietic cell populations. The interactomes were found to be highly enriched for proteins encoded by genes specifically expressed in HSCs relative to their differentiated progeny. Our data suggest a heretofore unappreciated similarity between regulatory modules in the brain and HSCs, offering a new strategy for novel gene discovery in both systems.