On 2017 Sep 18, Martine Crasnier-Mednansky commented:

The model for the chitin catabolic cascade indicates GlcNAc oligomers are degraded in the periplasm to ABC-transported (GlcNAc)2 and PTS-transported GlcNAc (figure 5 in Park JK, 2002 for the original model). The authors used (GlcNAc)4 and, because Enzyme IIA^Glc was largely phosphorylated in the presence of (GlcNAc)4, proposed there was "some mechanism for which chitin oligosaccharides escape from degradation into GlcNAc in the periplasmic space". If such mechanism occurs under the authors’ experimental conditions, it precludes any major PTS-transport effects on the chitin cascade, i.e. via dephosphorylation of Enzyme IIA^Glc during GlcNAc transport.

Working with Vibrio furnissii, Keyhani NO, 1996 argued, "since (GlcNAc)2 is an important inducer in the cascade, it must resist hydrolysis in the periplasm", and further provided an explanation for the stability of (GlcNAc)2 in the periplasm, particularly in sea water. It may well be that the rapid catabolism of (GlcNAc)2 is 'free' from any PTS control, and as such the cAMP necessary for the chitin cascade is provided.

On 2017 Sep 18, Martine Crasnier-Mednansky commented:

The model for the chitin catabolic cascade indicates GlcNAc oligomers are degraded in the periplasm to ABC-transported (GlcNAc)2 and PTS-transported GlcNAc (figure 5 in Park JK, 2002 for the original model). The authors used (GlcNAc)4 and, because Enzyme IIA^Glc was largely phosphorylated in the presence of (GlcNAc)4, proposed there was "some mechanism for which chitin oligosaccharides escape from degradation into GlcNAc in the periplasmic space". If such mechanism occurs under the authors’ experimental conditions, it precludes any major PTS-transport effects on the chitin cascade, i.e. via dephosphorylation of Enzyme IIA^Glc during GlcNAc transport.

Working with Vibrio furnissii, Keyhani NO, 1996 argued, "since (GlcNAc)2 is an important inducer in the cascade, it must resist hydrolysis in the periplasm", and further provided an explanation for the stability of (GlcNAc)2 in the periplasm, particularly in sea water. It may well be that the rapid catabolism of (GlcNAc)2 is 'free' from any PTS control, and as such the cAMP necessary for the chitin cascade is provided.