TABLE 2

Characterization of WS- mutants by physical mapping and sequence analysis

GroupMutantSpeI
RFa
Linking
RFb
GeneProposed functionComplementation
by pCSA/Bc
Congo
Redd
IWS-4A18.5 KpnIwspRResponse regulator--
IIWS-1H115.8 ClaIwssASpatial localization+-
WS-13H115.8 ClaIwssBCellulose synthase subunit+-
WS-22H115.8 ClaIwssCCellulose synthase subunit+-
WS-15H115.8 ClaIwssDEndoglucanase (cellulase)+-
WS-25H115.8 ClaIwssECellulose synthase subunit+-
IIIWS-18H18.6 ClaIwssFUnknown function++
WS-6H18.6 ClaIwssHPolymer modification++
WS-9H18.6 ClaIwssHPolymer modification++
IVWS-12T7.4 KpnIpgiAPhosphoglucose isomerase-±
VWS-39A9.4 KpnImreBMurien biosynthesis-+
VIWS-5ND13.6 ClaIeNDND-+
  • ND, not determined.

  • a Identity of SpeI restriction fragment containing the transposon (see Rainey and Bailey 1996).

  • b Smallest ApaI, ClaI, or KpnI linking fragment (size, in kilobases, includes 2.2 kb of mini-Tn5-km). SalI and SphI digests were also used to determine the number of unique mutants/replicate mutants within each group.

  • c Complementation of genetic lesion by cosmids pCSA and pCSB: -, not complemented; +, complemented.

  • d Scored after growth of colonies on KB or LB agar supplemented with Congo Red: -, no uptake of dye; +, uptake of dye; ±, uptake of dye on LB, but not KB agar.

  • e Southern analysis indicates that WS-5 is not linked to any other mutants.