EC Number |
General Information |
Reference |
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2.3.1.4 | malfunction |
the mutant called lignescens, a temperature-sensitive mutant that exhibits ectopic lignin deposition and growth defects under high-temperature conditions, is due to single base transition G68S in glucosamine-6-phosphate N-acetyltransferase. When exposed to the restrictive temperature, the mutant strain contains a significantly smaller amount of UDP-GlcNAc than the wild type. The growth defects and ectopic lignification of the mutant are suppressed by the addition of UDP-GlcNAc. N-glycans are reduced and luminal binding protein 3, a typical UPR gene, is expressed in the mutant strain at the restrictive temperature. Treatment with UPR-inducing reagents phenocopies the mutant |
720693 |
2.3.1.4 | physiological function |
a bloodstream-form of Trypanosoma brucei GNA1 conditional null mutant is unable to sustain growth in vitro under nonpermissive conditions. Poly-N-acetyllactosamine structures are greatly reduced in the mutant under nonpermissive conditions and the glycosylation profile of the principal parasite surface coat component, the variant surface glycoprotein, is modified |
719382 |
2.3.1.4 | physiological function |
biosynthetic pathway for synthesis of UDP-N-acetylglucosamine displays multiple regulation points such as regulation by the NagB enzyme, glmS RNA specific degradation through the possible participation of a glmS riboswitch mechanism, regulation of the glucosamine-1-phosphate acetyltransferase/N-acetylglucosamine-1-phosphate uridyltransferase activity probably by end product inhibition and transcription of glucosamine-1-phosphate acetyltransferase/N-acetylglucosamine-1-phosphate uridyltransferase |
719019 |
2.3.1.4 | physiological function |
lack of GNA1 influences cell adhesion and restoration of its function rescues the biological defect |
757009 |
2.3.1.4 | physiological function |
the GNA1 gene plays an essential role for the survival of the parasite, least during Plasmodium falciparum asexual blood stages |
758433 |