Cooperation of β-galactosidase and β-N-acetylhexosaminidase from bifidobacteria in assimilation of human milk oligosaccharides with type 2 structure

Cooperation of β-galactosidase and β-N-acetylhexosaminidase from bifidobacteria in assimilation of human milk oligosaccharides with type 2 structure
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DOI:
10.1093/glycob/cwq101
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发表时间:
2010-11-01
期刊:
影响因子:
4.3
通讯作者:
Yamamoto, Kenji
Yamamoto, Kenji
中科院分区:
生物学3区
文献类型:
--
作者:
Miwa, Mika;Horimoto, Tomohiro;Yamamoto, Kenji

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双歧杆菌在母乳喂养的婴儿的肠道中占主导地位,并为宿主提供健康益处。母乳低聚糖(HMO)被认为是肠道双歧杆菌最重要的生长因子之一。HMO含有两种主要的核心四糖结构:乳糖-N-四糖(Gal β 1-3GlcNAc β 1-3Gal β 1-4Glc; 1型链)和乳糖-N-新四糖(Gal β 1-4GlcNAc β 1-3Gal β 1-4Glc; 2型链)。我们以前确定了独特的代谢途径乳-N-四糖在两歧双歧杆菌。在这里,我们阐明了乳-N-新四糖在同一双歧杆菌中的降解途径。我们克隆了一个β-半乳糖苷酶(BbgIII)和两个β-N-乙酰氨基己糖苷酶(BbhI和BbhII),所有这些都是细胞外膜结合酶。重组BbgIII水解乳糖-N-新四糖为半乳糖和乳糖-N-三糖II,重组BbhI催化乳糖-N-三糖II水解为GlcNAc和乳糖,而BbhII不催化。由于BbgIII和BbhI分别对乳糖-N-新四糖和乳糖-N-三糖II具有高度特异性,因此它们可能在降解HMO中的2型寡糖中发挥重要作用。
Bifidobacteria are predominant in the intestines of breast-fed infants and offer health benefits to the host. Human milk oligosaccharides (HMOs) are considered to be one of the most important growth factors for intestinal bifidobacteria. HMOs contain two major structures of core tetrasaccharide: lacto-N-tetraose (Gal beta 1-3GlcNAc beta 1-3Gal beta 1-4Glc; type 1 chain) and lacto-N-neotetraose (Gal beta 1-4GlcNAc beta 1-3Gal beta 1-4Glc; type 2 chain). We previously identified the unique metabolic pathway for lacto-N-tetraose in Bifidobacterium bifidum. Here, we clarified the degradation pathway for lacto-N-neotetraose in the same bifidobacteria. We cloned one beta-galactosidase (BbgIII) and two beta-N-acetylhexosaminidases (BbhI and BbhII), all of which are extracellular membrane-bound enzymes. The recombinant BbgIII hydrolyzed lacto-N-neotetraose into Gal and lacto-N-triose II, and furthermore the recombinant BbhI, but not BbhII, catalyzed the hydrolysis of lacto-N-triose II to GlcNAc and lactose. Since BbgIII and BbhI were highly specific for lacto-N-neotetraose and lacto- N-triose II, respectively, they may play essential roles in degrading the type 2 oligosaccharides in HMOs.