The Myxococcus xanthus socE and csgA genes are regulated by the stringent response.

Disruption of the Myxococcus xanthus socE gene bypasses the requirement for the cell contact-dependent C-signalling system mediated by CsgA and restores fruiting body morphogenesis and spore differentiation. The socE gene has been identified by genetic complementation, cloned and sequenced. SocE is highly basic, unique and is predicted to be a soluble protein with a molecular size of 53. 6 kDa. The socE and csgA genes have opposite transcription patterns during the M. xanthus life cycle. socE expression is high in growing cells and declines during the early stages of development. Expression of csgA is low in vegetative cells and increases during development. socE transcription is negatively regulated by the stringent response, the major amino acid-sensing pathway in M. xanthus. A relA null mutation, which eliminates the stringent response, prevents the decline in socE expression normally observed at the onset of development. CsgA is positively regulated by the stringent response and is negatively regulated by socE. A relA mutation virtually eliminates developmental csgA expression. Expression of socE in Escherichia coli leads to a rapid loss of viability in relA- cells during stationary phase, suggesting a relationship with the stringent response.

The stringent response in Myxococcus xanthus is regulated by SocE and the CsgA C-signaling protein.

Myxococcus xanthus fruiting body development is induced by amino acid limitation. The decision to grow or develop is established by the RelA-dependent stringent response and A-signaling. We identified two new members of this regulatory hierarchy, socE and the C-signaling gene csgA. SocE depletion arrests growth and induces sporulation under conditions that normally favor growth as well as curtailing DNA and stable RNA synthesis, inhibiting cell elongation, and inducing accumulations of the stringent nucleotides ppGpp and pppGpp [(p)ppGpp]. This system separates C-signaling, which does not occur under these conditions, from CsgA enzyme activity. Amino acid substitutions in the CsgA coenzyme binding pocket or catalytic site eliminate growth arrest. relA mutation also eliminates growth arrest. Eleven pseudorevertants selected for growth following SocE depletion contained mutations in csgA or relA. These results suggest that CsgA induces the stringent response and while SocE inhibits it. Unlike the csgA mutant, wild-type and socE csgA cells maintained high levels of (p)ppGpp throughout development. We suggest that CsgA maintains growth arrest throughout development to divert carbon from A-signaling and other sources into developmental macromolecular synthesis.

LIS-lnterlink-connecting laboratory information systems to remote primary health-care centres via the Internet.

A pilot study was performed to evaluate the feasibility of using the Internet to securely deliver patient laboratory results, and the system has subsequently gone into routine use in Poland. The system went from design to pilot and then to live implementation within a four-month period, resulting in the LIS-Interlink software product. Test results are retrieved at regular intervals from the BioLink(TM) LIS (Laboratory Information System), encrypted and transferred to a secure area on the Web server. The primary health-care centres dial into the Internet using a local-cell service provided by Polish Telecom (TP), obtain a TCP/IP address using the TP DHCP server, and perform HTTP 'get' and 'post' operations to obtain the files by secure handshaking. The data are then automatically inserted into a local SQL database (with optional printing of incoming reports)for cumulative reporting and searching functions. The local database is fully multi-user and can be accessed from different clinics within the centres by a variety of networking protocols.