Characterization of the ksgA gene of Escherichia coli determining kasugamycin sensitivity

Autogenous regulation of the Escherichia coli ksgA gene at the level of translation

“…4) are, as mentioned in Results, most readily explained in terms of concentration. They probably also explain our previous conclusion that the ksgA system was not autoregulated (24). It should be mentioned that all our in vivo analyses have been performed with a highly sensitive immunoassay.…”

“…We have cloned and sequenced this gene and the flanking regions (23,24). The gene, located at 1 min on the E. coli chromosome, is preceded by a weak promoter, and the mRNA is translated despite the absence of a recognizable ribosomal binding site (3,24). Here we show that the gene is subject to autogenous regulation at the translational level, despite the fact that our previous studies showed no evidence for this (24).…”

Autogenous regulation of the Escherichia coli ksgA gene at the level of translation

“…4) are, as mentioned in Results, most readily explained in terms of concentration. They probably also explain our previous conclusion that the ksgA system was not autoregulated (24). It should be mentioned that all our in vivo analyses have been performed with a highly sensitive immunoassay.…”

“…We have cloned and sequenced this gene and the flanking regions (23,24). The gene, located at 1 min on the E. coli chromosome, is preceded by a weak promoter, and the mRNA is translated despite the absence of a recognizable ribosomal binding site (3,24). Here we show that the gene is subject to autogenous regulation at the translational level, despite the fact that our previous studies showed no evidence for this (24).…”

Antibiotic tolerance, persistence, and resistance of the evolved minimal cell, Mycoplasma mycoides JCVI-Syn3B

“…The first one is in the ksgA gene, which encodes a methylase that modifies 16S rRNA, and inhibition of this protein by the antibiotic kasugamycin causes susceptibility. Therefore, when ksgA is inactivated, cells became kasugamycin-resistant ( van Gemen et al., 1987 ; Mariscal et al., 2018 ). We reasoned that the nonsynonymous mutation in ksgA in PK07 makes the protein inactive and able to confer kasugamycin resistance.…”

Antibiotic tolerance, persistence, and resistance of the evolved minimal cell, Mycoplasma mycoides JCVI-Syn3B

“…The first one is in the ksgA gene, which encodes a methylase that modifies 16S rRNA, and inhibition of this protein by the antibiotic kasugamycin causes susceptibility. Therefore, when ksgA is inactivated, cells became kasugamycin-resistant (Mariscal et al, 2018; van Gemen et al, 1987). We reasoned that the nonsynonymous mutation in ksgA in PK07 makes the protein inactive and able to confer kasugamycin resistance.…”

Autogenous regulation of the Escherichia coli ksgA gene at the level of translation

“…4) are, as mentioned in Results, most readily explained in terms of concentration. They probably also explain our previous conclusion that the ksgA system was not autoregulated (24). It should be mentioned that all our in vivo analyses have been performed with a highly sensitive immunoassay.…”

“…We have cloned and sequenced this gene and the flanking regions (23,24). The gene, located at 1 min on the E. coli chromosome, is preceded by a weak promoter, and the mRNA is translated despite the absence of a recognizable ribosomal binding site (3,24). Here we show that the gene is subject to autogenous regulation at the translational level, despite the fact that our previous studies showed no evidence for this (24).…”

Antibiotic tolerance, persistence, and resistance of the evolved minimal cell, Mycoplasma mycoides JCVI-Syn3B

“…The first one is in the ksgA gene, which encodes a methylase that modifies 16S rRNA, and inhibition of this protein by the antibiotic kasugamycin causes susceptibility. Therefore, when ksgA is inactivated, cells became kasugamycin-resistant ( van Gemen et al., 1987 ; Mariscal et al., 2018 ). We reasoned that the nonsynonymous mutation in ksgA in PK07 makes the protein inactive and able to confer kasugamycin resistance.…”

Antibiotic tolerance, persistence, and resistance of the evolved minimal cell, Mycoplasma mycoides JCVI-Syn3B

“…The first one is in the ksgA gene, which encodes a methylase that modifies 16S rRNA, and inhibition of this protein by the antibiotic kasugamycin causes susceptibility. Therefore, when ksgA is inactivated, cells became kasugamycin-resistant (Mariscal et al, 2018; van Gemen et al, 1987). We reasoned that the nonsynonymous mutation in ksgA in PK07 makes the protein inactive and able to confer kasugamycin resistance.…”

Autogenous regulation of the Escherichia coli ksgA gene at the level of translation

“…4) are, as mentioned in Results, most readily explained in terms of concentration. They probably also explain our previous conclusion that the ksgA system was not autoregulated (24). It should be mentioned that all our in vivo analyses have been performed with a highly sensitive immunoassay.…”

“…We have cloned and sequenced this gene and the flanking regions (23,24). The gene, located at 1 min on the E. coli chromosome, is preceded by a weak promoter, and the mRNA is translated despite the absence of a recognizable ribosomal binding site (3,24). Here we show that the gene is subject to autogenous regulation at the translational level, despite the fact that our previous studies showed no evidence for this (24).…”

Antibiotic tolerance, persistence, and resistance of the evolved minimal cell, Mycoplasma mycoides JCVI-Syn3B

“…The first one is in the ksgA gene, which encodes a methylase that modifies 16S rRNA, and inhibition of this protein by the antibiotic kasugamycin causes susceptibility. Therefore, when ksgA is inactivated, cells became kasugamycin-resistant ( van Gemen et al., 1987 ; Mariscal et al., 2018 ). We reasoned that the nonsynonymous mutation in ksgA in PK07 makes the protein inactive and able to confer kasugamycin resistance.…”

Antibiotic tolerance, persistence, and resistance of the evolved minimal cell, Mycoplasma mycoides JCVI-Syn3B

“…The first one is in the ksgA gene, which encodes a methylase that modifies 16S rRNA, and inhibition of this protein by the antibiotic kasugamycin causes susceptibility. Therefore, when ksgA is inactivated, cells became kasugamycin-resistant (Mariscal et al, 2018; van Gemen et al, 1987). We reasoned that the nonsynonymous mutation in ksgA in PK07 makes the protein inactive and able to confer kasugamycin resistance.…”