A novel bacterial putrescine utilization pathway was discovered. Seven genes, the functions of whose products were not known, are involved in this novel pathway. Five of them encode enzymes that catabolize putrescine; one encodes a putrescine importer, and the other encodes a transcriptional regulator. This novel pathway involves six sequential steps as follows: 1) import of putrescine; 2) ATP-dependent ␥-glutamylation of putrescine; 3) oxidization of ␥-glutamylputrescine; 4) dehydrogenation of ␥-glutamyl-␥-aminobutyraldehyde; 5) hydrolysis of the ␥-glutamyl linkage of ␥-glutamyl-␥-aminobutyrate; and 6) transamination of ␥-aminobutyrate to form the final product of this pathway, succinate semialdehyde, which is the precursor of succinate.

Some amino acids and peptides, which have low solubility in water, become much more soluble following gamma-glutamylation. Compounds become more stable in the blood stream with gamma-glutamylation. Several gamma-glutamyl compounds are known to have favorable physiological effects on mammals. Gamma-glutamylation can improve taste and can stabilize glutamine in aqueous solution. Because of such favorable features, gamma-glutamyl compounds are very attractive. However, only a small number of gamma-glutamyl amino acids have been studied although many other gamma-glutamyl compounds may have characteristics that will benefit humans. This is mainly because gamma-glutamyl compounds have not been readily available. An efficient and simple method of producing various gamma-glutamyl compounds, especially gamma-glutamyl amino acids, using bacterial gamma-glutamyltranspeptidase has been developed. With this method, modifications of reactive groups of the substrate and energy source such as ATP are not required, and a wide-range of gamma-glutamyl compounds can be synthesized. Moreover, bacterial gamma-glutamyltranspeptidase, a catalyst for this method, is readily available from the strain over-producing this enzyme. The superiority of producing gamma-glutamyl compounds with bacterial gamma-glutamyltranspeptidase over other methods of production is discussed.

Motivation facilitates recovery after neuronal damage, but its mechanism is elusive. It is generally thought that the nucleus accumbens (NAc) regulates motivation-driven effort but is not involved in the direct control of movement. Using causality analysis, we identified the flow of activity from the NAc to the sensorimotor cortex (SMC) during the recovery of dexterous finger movements after spinal cord injury at the cervical level in macaque monkeys. Furthermore, reversible pharmacological inactivation of the NAc during the early recovery period diminished high-frequency oscillatory activity in the SMC, which was accompanied by a transient deficit of amelioration in finger dexterity obtained by rehabilitation. These results demonstrate that during recovery after spinal damage, the NAc up-regulates the high-frequency activity of the SMC and is directly involved in the control of finger movements.

In skeletogenic mesenchyme, SOXC proteins enter the APC–Axin destruction complex to inhibit β-catenin phosphorylation by GSK3 and thereby synergize with canonical WNT signaling to inhibit chondrogenesis.