Further characterization of Dothistromin genes in the fungal forest pathogen Dothistroma septosporum : a thesis presented in partial fulfilment of the requirements for the degree of Masters of Science in Molecular Genetics at Massey University, Palmerston North, New Zealand

Dothistroma septosporum is a forest pathogen that causes a disease called Dothistroma needle blight. The symptoms are thought to be due to the accumulation of dothistromin toxin produced by D. septosporum. Dothistromin is characterized as a difuranoanthraquinone and shows remarkable similarity to the aflatoxin (AF) and sterigmatocystin (ST) precursor versicolorin B. The similar structure to AF/ST suggests that dothistromin biosynthesis shares biosynthetic steps with the AF/ST pathway. The AF gene cluster in Aspergillus parasiticus and ST gene cluster in A. nidulans have been well characterized. Nine putative dothistromin biosynthetic genes have been identified. One of them, dotA was previously characterized by gene disruption and shown to have a similar function to homologous genes in AF/ST biosynthesis. Two additional putative dothistromin biosynthetic genes, pksA and epoA, were characterized by gene disruption in this study. The inability of the pksA mutants to produce dothistromin indicated that the pksA is a key gene in dothistromin biosynthesis. The feeding of intermediates confirmed that pksA gene product is required for a very early step of dothistromin biosynthesis. The pksA mutants also showed reduced sporulation compared to wildtype, suggesting a relationship between dothistromin production and sporulation. The epoA gene replacements were also obtained successfully by homologous recombination. Both Southern blot and northern hybridization confirmed that the epoA gene was disrupted. However, the epoA mutants did not show any difference to the wild type in three analyses (growth rate, sporulation rate, dothistromin biosynthesis). However it was not possible to rule out a role for EpoA at a very late stage of dothistromin biosynthesis. RACE analysis of the nine identified dothistromin genes characterized the transcription start and stop sites of the genes. Analyzing the putative regulatory protein binding motifs in the untranscribed region of the genes provided clues about the regulation of dothistromin biosynthesis and suggested there might be an aflR-like gene that governs dothistromin biosynthesis. Both the pksA gene disruption and the RACE results suggested that the dothistromin biosynthetic pathway is homologous to that of AF/ST biosynthesis. Further work on the dothistromin gene cluster will help us to understand the evolution of fungal toxin gene clusters

Proposal for realizing a multiqubit tunable phase gate of one qubit simultaneously controlling n target qubits using cavity QED

We propose a way to realize a multiqubit tunable phase gate of one qubit simultaneously controlling n target qubits with atoms in cavity QED. In this proposal, classical pulses interact with atoms outside a cavity only, thus the experimental challenge of applying a pulse to an intra-cavity single atom without affecting other atoms in the same cavity is avoided. Because of employing a first-order large detuning, the gate can be performed fast when compared with the use of a second-order large detuning. Furthermore, the gate operation time is independent of the number of qubits. This proposal is quite general, which can be applied to various superconducting qubits coupled to a resonator, NV centers coupled to a microsphere cavity or quantum dots in cavity QED.Comment: 4 pages, 5 figures, accepted by Phys. Rev.

Design of a multiple bloom filter for distributed navigation routing

Unmanned navigation of vehicles and mobile robots can be greatly simplified by providing environmental intelligence with dispersed wireless sensors. The wireless sensors can work as active landmarks for vehicle localization and routing. However, wireless sensors are often resource scarce and require a resource-saving design. In this paper, a multiple Bloom-filter scheme is proposed to compress a global routing table for a wireless sensor. It is used as a lookup table for routing a vehicle to any destination but requires significantly less memory space and search effort. An error-expectation-based design for a multiple Bloom filter is proposed as an improvement to the conventional false-positive-rate-based design. The new design is shown to provide an equal relative error expectation for all branched paths, which ensures a better network load balance and uses less memory space. The scheme is implemented in a project for wheelchair navigation using wireless camera motes. © 2013 IEEE

Transition from Initial Hypoactivity to Hyperactivity in Cortical Layer V Pyramidal Neurons after Traumatic Brain Injury In Vivo

Traumatic brain injury (TBI) often results in structural damage and a loss of neurons that is commonly accompanied by early changes in neuronal electrical activity. Loss of neuronal activity has been hypothesized to contribute to post-traumatic epileptogenesis through the regulation of homeostatic plasticity. The existence of activity loss in cortical neurons after TBI and its subsequent transition into hyperactivity over time is not well characterized, however, particularly in models of TBI in vivo. In the current study, changes in neuronal activity in the primary motor cortex after moderate controlled cortical impact (CCI) in mice were studied using a single-unit recording technique in vivo. Recordings were made at different time points after CCI from cortical layer V pyramidal neurons that were within 1-2 mm from the anterior edge of the injured foci. Within 1-4 h after CCI, the frequency of spontaneous single-unit activity depressed significantly, with the mean firing frequency decreasing from 2.59 ± 0.18 Hz in the sham group to 1.05 ± 0.20 Hz of the injured group. The firing frequencies recovered to the normal level at 1 day and 7 days post-CCI, but became significantly higher at 3 days and 14 days post-CCI. The results suggest that TBI caused initial loss of activity in neurons of the perilesional cortical region, which was followed by compensatory recovery and enhancement of activity. These time-dependent changes in neuronal activity may contribute to the development of hyperexcitability through homeostatic activity regulation