Effects of laryngeal nerve transection on squirrel monkey calls

Summary Six squirrel monkeys (Saimiri sciureus) were implanted with intracerebral electrodes yielding specific call types when electrically stimulated. Two animals then received bilateral transection of the recurrent nerve; in another two animals the external branch of the superior laryngeal nerve was cut bilaterally; two further animals received unilateral transection of either the recurrent or the external laryngeal nerve. In one animal with both recurrent nerves cut, the external laryngeal nerves were cut in addition 3 months later. The vocal changes caused by these transections were observed and can be summarized as follows:Unilateral interruption of the recurrent nerve causes only minor disturbances which are limited to low-pitched sounds. Bilateral interruption of the same nerve leads to a reduction of maximal intensities and durations in general. Whereas the frequency-time structure is severely disorganized in all harmonic calls with a fundamental below 1 kHz and all non-harmonic, noise-like calls, it remains unaffected in harmonic calls with a fundamental above 1 kHz. Unilateral transection of the external laryngeal nerve causes a drop of fundamental frequency in high-pitched calls to almost half. Bilateral transection of the same nerve abolishes all calls with a fundamental above 1 kHz. In wide-band frequency calls it is followed by a shift of main energy towards lower frequencies. Low-pitched harmonic as well as noise-like calls remain normal. Cutting both external laryngeal nerves in addition to recurrent nerves is followed by loss of all sounds except one coughing-like, abnormal call. All animals with transection of the external laryngeal nerve show recovery of the high-pitched calls which seems to be due to new innervation of the cricothyroid muscle from the pharyngeal plexus.     

Potential of ultraviolet radiation for control of american cockroach populations

Populations of Periplaneta americana (L.) were exposed for 8–20 week periods in specially designed rooms to 254 nm UV at low intensity (50–115 ergs sec^–1cm^–2), high intensity (160–220 ergs sec^–1cm^–2), or to white light. The rooms contained tables and chairs to simulate occupied space, with food and water placed in positions exposed to UV radiation. General irradiation (where the whole room was exposed to UV) at 115 ergs sec^–1cm^–2 and above was effective in producing high mortality in all stages except 8–10th instar nymphs and adults. Hot-spots irradiation (where UV lamps were placed behind table and chair harborages) produced high mortality only in 1 st-3rd instar nymphs which would result in slower elimination of a population. Crude aggregation pheromone was not successful in holding cockroaches close to radiation sources or substantially increasing mortality under the conditions of the experiments.

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Zusammenfassung Populationen von Periplaneta americana (L.), die hinsichtlich ihrer Alterszusammensetzung (2.–3.; 5–6.; 8.–10. und adultes Stadium) und der Anzahlen in jedem Stadium festgelegt waren, wurden für 8–20 Wochenperioden in speziell dafür entworfenen Räumen einer 254 nm UV-Bestrahlung mit geringer (50–115 erg sec^–1cm^–2) oder hoher (160–220 erg sec^–1cm^–2) Intensität oder weißem Licht (als Kontrolle) ausgesetzt. Die Räume enthielten Tische und Stühle, um bewohnten Raum mit natürlichen Zufluchtsstätten mit Nahrung und Wasser an Stellen, die der UV-Bestrahlung unterlagen, zu simulieren. Ganzraumbestrahlung mit 115 erg sec^–1cm^–2 und darüber erzeugte hohe Mortalität bei 1.–3. und 5.–6.-Larvenstadien, örtliche Bestrahlung (UV-Lampen hinter Tisch- und Stuhl-Zufluchtsstätten) dagegen nur beim 1.–3.-Stadium, was zu einer langsameren Ausrottung einer Population führen würde. Ungereinigtes Aggregationspheromon als Zusatz, um Schaben dicht an die UV-Quellen zu locken und sie hier zu halten, war offenbar unwirksam, da eben die Mortalität nicht signifikant zunahm. Dieses Versagen war in erster Linie auf die Konkurrenz mit der Fülle von natürlichem Pheromon, das von den gewohnten Zufluchtsstätten ausging, zurückzuführen, verbunden mit der dem UV-Licht innewohnenden Abschreckung. Dennoch darf man annehmen, daß UV-Bestrahlung einen bedeutsamen Wert für die Verhinderung eines Populationswachstums (durch Ausschalten junger Larvenstadien) besitzt, besonders dort, wo chemische Bekämpfung aus Gesundheits- und Sicherheitsgründen oder wegen gesetzlichen Einschränkungen nur begrenzt möglich ist.

     

Localization of phytochrome in oats by electron microscopy

Phytochrome was localized by immunoelectron microscopy in cells of the coleoptile tip of etiolated and irradiated oat (Avena sativa L., cv. Konata) seedlings. By using ultrathin frozen sections and immunopurified, monospecific antibodies, both the sensitivity and resolution of the immunocytochemical assay were increased. The results with etiolated plants agree with and extend previously published data. A brief red light illumination caused the redistribution of phytochrome from a diffuse to a more particulate appearance. Areas that accumulated phytochrome were identified as small vacuoles into which phytochrome was sequestered following illumination. In seedlings illuminated for several hours and in normal light-grown plants, the cellular distribution of phytochrome is qualitatively similar to that of nonirradiated, dark-grown material, except that in green plants the nucleus shows a positive immunocytochemical reaction.     

Phytochrome Modification and Light-enhanced, In Vivo-induced Phytochrome Pelletability

Phytochrome that was induced by red irradiation in vivo to pellet with subcellular material and that was released from the pellet by removal of divalent cations exhibited altered characteristics. Compared to phytochrome extracted in a soluble red-absorbing form from etiolated tissue, pelleted and released phytochrome, which was also assayed in the red-absorbing form even though pelleted in the far-red-absorbing form, showed 50% greater micro complement fixation activity, eluted closer to the void volume of a Sephadex G-200 column, and electrophoresed more slowly on sodium dodecyl sulfate-polyacrylamide gels. Data presented here document that phytochrome pelleted in the far-red-absorbing form differs from soluble phytochrome extracted from nonirradiated tissue. These data, however, do not permit the conclusion that there is a causal relationship between pelletability and phytochrome modification.     

Electron spin resonance study of the role of NO . catalase in the activation of guanylate cyclase by NaN3 and NH2OH. Modulation of enzyme responses by heme proteins and their nitrosyl derivatives.

The role of NO . catalase in the activation of partially purified soluble guanylate cyclase of rat liver by NaN3 and NH2OH was examined by electron spin resonance (ESR) spectroscopy. Equilibration of bovine liver catalase with NO resulted in formation of a paramagnetic species exhibiting a three-line ESR spectrum similar to that of NO . catalase. This paramagnetic complex produced concentration-dependent stimulation of preparations of partially purified guanylate cyclase that were devoid of detectable endogenous heme content. The stimulation of partially purified guanylate cyclase by NO . catalase was similar to that obtained with NO . hemoglobin and with NO . cytochrome P-420 prepared by reaction of hepatic microsomes of phenobarbital-treated rats with NO. By contrast, these same enzyme preparations did not respond to NO or catalase alone. Addition of hematin or hemoglobin plus a reducing agent to purified guanylate cyclase restored enzyme responsiveness to NO and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), but not to NaN3 or NH2OH. Responses to the latter agents were restored by catalase and potentiated by a H2O2-generating system. Formation of the NO . catalase complex was evident by ESR spectroscopy in test solutions containing NaN3 or nh2oh, catalase, and a glucose-glucose oxidase, H2O2-generating system. The presence of NO . catalase correlated well with the ability of test solutions to activate purified guanylate cyclase. These results provide evidence for catalase-dependent NO generation from NaN3 and NH2OH under conditions leading to guanylate cyclase activation. Preformed NO . hemoglobin or NO . cytochrome P-420 also activated heme-deficient partially purified guanylate cyclase. The ability of several preformed NO . heme protein complexes, but not NO, to stimulate heme-deficient guanylate cyclase supports the concept that formation of the paramagnetic nitrosyl . heme complex, mediated by either enzymatic or nonenzymatic reactions, is a common and essential step in the process by which NO or NO-forming compounds activate guanylate cyclase. In the absence of the NO ligand, both hemoglobin and catalase suppress the stimulatory effects of the corresponding NO . heme proteins on guanylate cyclase. Release of each heme protein from the NO . heme protein complex occurs more rapidly under aerobic compared to anaerobic conditions. However, hemoglobin is approximately 2000 times more effective as an inhibitor of NO . hemoglobin stimulation of guanylate cyclase than is catalase as an inhibitor of NO . catalase action. This finding may explain the more pronounced decline in the rate of cGMP generation in air in the presence of NO . hemoglobin compared to NO . catalase. The results imply that guanylate cyclase responses to activators that can form NO are determined by both the stimulatory activity of the endogenous heme acceptors of NO and the relative inhibitory effects of the unliganded heme proteins present.     

Subunit 4 of the 26 S protease is a member of a novel eukaryotic ATPase family.

Ubiquitinated proteins are degraded by a 26 S ATP-dependent protease. SDS-polyacrylamide gel electrophoresis analysis of the purified 26 S enzyme reveals more than 20 polypeptides ranging in apparent molecular masses from 20 to 110 kDa. Although many of the subunits smaller than 30 kDa are members of the multicatalytic protease family, the identity and function of the larger polypeptides have remained unknown. We report here the cDNA sequence for subunit 4, a 51-kDa chain of the 26 S protease. Subunit 4 belongs to a recently identified eukaryotic ATPase family, which includes proteins involved in peroxisome formation, secretion, and human immunodeficiency virus gene expression. Subunit 4 also shows weak similarity to ClpA, the ATP-binding subunit of the Escherichia coli protease, Clp.     

Evidence that the hormone-binding domain of the mouse glucocorticoid receptor directly represses DNA binding activity in a major portion of receptors that are "misfolded" after removal of hsp90.

After dissociation of cytosolic heteromeric glucocorticoid receptor complexes by steroid, salt, and other methods, only 35-60% of the dissociated receptors can bind to DNA-cellulose. The DNA-binding and non-DNA-binding forms of the dissociated receptors have the same Mr and are phosphorylated to the same extent (Tienrungroj, W., Sanchez, E. R., Housley, P. R., Harrison, R. W., and Pratt, W. B. (1987) J. Biol. Chem. 262, 17347-17349). The basis for the different DNA-binding activities is unknown, but the DNA-binding fraction of the receptor has a more basic pI than the non-DNA-binding fraction (Smith, A. C., Elsasser, M. S., and Harmon, J. M. (1986) J. Biol. Chem. 261, 13285-13292). We have separated the non-DNA-binding state of the receptor from the DNA-binding state and then cleaved it with trypsin and chymotrypsin. We find that the 15-kDa tryptic fragment derived from the non-DNA-binding state of the dissociated receptor is fully competent in binding DNA, whereas the 42-kDa chymotryptic fragment containing both the hormone-binding and DNA-binding domains does not bind DNA. Trypsin cleavage of the molybdate-stabilized untransformed receptor also yields a 15-kDa fragment that is fully competent in binding DNA. Reducing agents do not restore DNA-binding to the non-DNA-binding fraction of the receptor and the hormone-binding domain can be separated from the DNA-binding domain on nonreducing gel electrophoresis. These results argue that the two domains are not linked by disulfide bridges, and they are consistent with the proposal that there are two least energy states of folding after dissociation of hsp90. A significant portion of the receptors is "misfolded" in such a manner that the steroid binding domain is directly preventing DNA-binding activity.