TABLE 2.

Properties of fimH mutants

Lesion locationa (nt)	No. of isolatesb	Morphologic classc	Representative fimH allele (strain no.)	Type of lesion, amino acid change if missense (amino acid position)d	Phenotype or other relevant properties
56	5	I	fimH241 (ORN160)	Missense, Ala (−3)→asp	Amino acid change in signal sequence near processing site
62	3e	II	fimH236 (ORN164)	Missense, Ser (−1)→Leu	Amino acid change in signal sequence at processing site
194	1	I	fimH244 (ORN165)	Missense, Cys (44)→Tyr	Amino acid change in first of four cysteine residues
236	1	I	fimH205 (ORN157)	Missense, Leu (58)→Arg	Amino acid change produces a conditional erythrocyte agglutination phenotype
291	1f	III	fimH208 (ORN158)	Frameshift, deletion of 1 nucleotide	Frameshift lesion predicts a truncated protein approximately 40% of normal size

^aNucleotide (nt) residue altered. Refer to Fig. 1 for coordinates. The parental fimH allele is identical to that of the fully sequenced E. coli K-12 strain MG1655, referenced in the text. 

^bNumber of isolates refers to the number of independently isolated fimH mutants having the same mutation by DNA sequencing and recombination analysis. Five identical mutant alleles were found at position 56 (fimH241, fimH229, fimH222, fimH247, and fimH246 [13]). Three identical alleles were found at position 62 (fimH336, fimH204, and fimH218 [13]). 

^cMorphologic class refers to the classes observed by Harris et al. (13). Class I mutants have normal-appearing pili, class II mutants have longer than normal pili, and class III mutants have fewer and longer pili. See text for additional details. 

^dSee Fig. 1 for base pair changes, lesion location, and amino acid position. 

^eOriginally, only one mutant having the representative allele (fimH236) was scored as being a class II mutant (13). Retrospective analysis of available electron micrographs revealed that at least one of the two additional mutants was simply overlooked in the original screen (data not shown). 

^fIn addition to strain ORN158, one additional mutant was scored as being a class III mutant in our original phenotypic screening (13). Upon examination of Southern blots using DNA encoding fimH as a probe, and PCR sequencing of the chromosomal fimH allele in this mutant, it was concluded that there had been an aberrant introduction of this allele into the chromosome (our unpublished observations).