Two Rhizobium phaseoli mutants, isolated previously by TnS mutagenesis, elicited infection threads which ceased development prematurely, usually within root hairs. These infection threads were wide, globular, and otherwise altered in morphology, compared with normal infection threads. Anatomy and division of the root cortical cells during initial stages of nodule morphogenesis appeared normal. However, later nodule differentiation deviated considerably from normal development, and release of bacteria from infection threads was not observed. In tryptone-yeast extract medium the mutants sedimented during growth in shaken cultures and formed rough colonies on agar. Electrophoresis of washed cultures solubilized in dodecyl sulfate revealed that the major carbohydrate band was absent from the mutants. The behavior of this carbohydrate in phenol-water extraction and gel chromatography, its apparent ketodeoxyoctonate content, and its susceptibility to mild acid hydrolysis suggested that it was a lipopolysaccharide. From the results of genetic crosses or reversion analysis, the defect in synthesizing this carbohydrate material and the defect in infection could be attributed to a single mutation in each mutant.Nitrogen-fixing root nodules appear on legumes only in the presence of bacteria of the genera Rhizobium and Bradyrhizobium. Several early events in nodule development are common to most legumes that have been studied (1, 27), including Phaseolus vulgaris (bean). In these legumes the bacteria invade curled, or otherwise deformed, root hairs (1,27). According to a theory best substantiated with soybean (1,5,37), the root hairs that will be invaded generally have not emerged from the developing root at the time of first bacterial contact. The presence of the bacteria causes the root hairs to curl as they develop (1). A bacterial colony at the root hair surface is thought to become trapped in a pocket created by this deformation, and from this pocket the bacteria penetrate the root hair cell wall (4,37). A wall of host origin is deposited between the invading bacteria and the involuted plasmalemma (4, 27, 37). The bacteria, this tubular wall, and associated material constitute an infection thread, which grows through the root hair cell into the root cortex. During the course of this infection sequence, active cell division commences in the root cortex (5, 27). As the nodule develops from this region of meristematic activity, bacteria eventually are released from the infection thread into some of the resulting host cells (26), but remain separated from the host cytoplasm by peribacteroid membranes (27) targeted genes have been characterized at the molecular level (11,12,15,31).In contrast to Nod-mutants, certain mutants of R. meliloti and R. phaseoli stimulate normal meristematic activity, but fail to elicit infection threads. In the nodulelike structures that result, little or no evident bacterial penetration is observed (13a, 17, 38). The mutations map in a plasmid other than the Sym plasmid (17, 23) and in the chromo...

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