A Trypanosoma brucei β3 glycosyltransferase superfamily gene encodes a β1-6 GlcNAc-transferase mediating N-glycan and GPI anchor modification

Duncan, Sheila L. B.; Nagar, Rupa; Damerow, Manuela; Yashunsky, Dmitry V.; Buzzi, Benedetta; Nikolaev, Andrei V.; Ferguson, Michael A. J.

doi:10.1016/j.jbc.2021.101153

Cited by 7 publications

(35 citation statements)

References 53 publications

(58 reference statements)

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“…However, whereas canonical GT16 GnTIIs work on GlcNAc 1 Man 3 GlcNAc 2 , GT67 TbGnTII can operate with nothing or anything substituting the 3-arm αMan residue. This also means that TbGnTI and TbGnTII can TbGT15) are according to [15,18]. Those TbGTs that appear in proteomics data are shown in Figure 3.…”

Section: Lineages 3 Andmentioning

confidence: 87%

“…The comparable motifs in the T. brucei genes are WG, Y(I,V,F)XKXDDD, and ED(A/V/I/L/M)(M/L)X(G/A). The GT67 family, therefore, appears to have diverged from the normal eukaryotic β3GT lineages and then expanded and evolved such that GT67 GTs can take the place of GT13 [17], GT14 [16], GT16 [18], GT31 [19] and GT49 [15] (and probably more) GT family members.…”

Section: Divergent and Convergent Evolution Of Gt67 Family Gtsmentioning

confidence: 99%

“…Here, we have performed similar analysis and included T. evansi [67], which does not differentiate to the PCF stage due to the absence of a mitochondrial genome, and T. gambiense, the human pathogenic strain closely related to T. b. brucei (Figure 2). We overlay and interpret this phylogenetic analysis with the available data on T. brucei GT67 functions [15][16][17][18][19] and on TbGT, TbOST and glycan-processing enzyme protein expression data from quantitative proteomics [68]. The latter expressed graphically in (Figure 3) using the tools in described in [69].…”

Section: Divergent and Convergent Evolution Of Gt67 Family Gtsmentioning

confidence: 99%

“…It adds βGlcNAc in 1-3 linkage to βGal residues. Lineage 6 contains the gene encoding TbGT10, which performs the same function as GT14 family GCNT, adding βGlcNAc in 1-6 linkage to βGal residues [18]. TbGT8 and TbGT10 are active in both BSF and PCF cells.…”

Section: Lineages 5 Andmentioning

confidence: 99%

“…However, this is not the case in T. brucei where several common GT families are missing and where a particular GT family (GT67), unique to kinetoplastids, has emerged and expanded. There are twenty of these genes in the T. brucei genome and, so far, the functions of five of them have been studied [15][16][17][18][19][20].…”

Section: Introductionmentioning

confidence: 99%

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Common and unique features of glycosylation and glycosyltransferases in African trypanosomes

Duncan

Ferguson

2022

Biochemical Journal

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Eukaryotic protein glycosylation is mediated by glycosyl- and oligosaccharyl-transferases. Here, we describe how African trypanosomes exhibit both evolutionary conservation and significant divergence compared with other eukaryotes in how they synthesise their glycoproteins. The kinetoplastid parasites have conserved components of the dolichol-cycle and oligosaccharyltransferases (OSTs) of protein N-glycosylation, and of glycosylphosphatidylinositol (GPI) anchor biosynthesis and transfer to protein. However, some components are missing, and they process and decorate their N-glycans and GPI anchors in unique ways. To do so, they appear to have evolved a distinct and functionally flexible glycosyltransferases (GT) family, the GT67 family, from an ancestral eukaryotic β3GT gene. The expansion and/or loss of GT67 genes appears to be dependent on parasite biology. Some appear to correlate with the obligate passage of parasites through an insect vector, suggesting they were acquired through GT67 gene expansion to assist insect vector (tsetse fly) colonisation. Others appear to have been lost in species that subsequently adopted contaminative transmission. We also highlight the recent discovery of a novel and essential GT11 family of kinetoplastid parasite fucosyltransferases that are uniquely localised to the mitochondria of Trypanosoma brucei and Leishmania major. The origins of these kinetoplastid FUT1 genes, and additional putative mitochondrial GT genes, are discussed.

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Section: Lineages 3 Andmentioning

confidence: 87%