Differential gene expression of β‐1,4‐galactosyltransferases I, II and V during mouse brain development

Nakamura, Nobuhiro; Yamakawa, Naomi; Satô, Takeshi; Tojo, Hideaki; Tachi, Chikashi; Furukawa, Kiyoshi

doi:10.1046/j.1471-4159.2001.00004.x

Cited by 46 publications

(30 citation statements)

References 39 publications

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“…We recently reported that ␤4GalT-II-deficient mice showed a marked reduction in levels of HNK-1 carbohydrate and impaired spatial memory, and the phenotypes are similar to those of GlcAT-P-deficient mice (19). Moreover, ␤4GalT-II is highly expressed in the brain although ␤4GalT-I is ubiquitous (39). These findings suggest intrinsic roles in vivo, although ␤4GalT-I and -II show the highest sequence similarity among ␤4GalTs.…”

Section: Discussionmentioning

confidence: 94%

Specific Enzyme Complex of β-1,4-Galactosyltransferase-II and Glucuronyltransferase-P Facilitates Biosynthesis of N-linked Human Natural Killer-1 (HNK-1) Carbohydrate

Kouno

Kizuka

Nakagawa

et al. 2011

Journal of Biological Chemistry

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Human natural killer-1 (HNK-1) carbohydrate is highly expressed in the nervous system and is involved in synaptic plasticity and dendritic spine maturation. This unique carbohydrate, consisting of a sulfated trisaccharide (HSO 3 -3GlcA␤1-3Gal␤1-4GlcNAc-), is biosynthesized by the successive actions of ␤-1,4-galactosyltransferase (␤4GalT), glucuronyltransferase (GlcAT-P and GlcAT-S), and sulfotransferase (HNK-1ST). A previous study showed that mice lacking ␤4GalT-II, one of seven ␤4GalTs, exhibited a dramatic loss of HNK-1 expression in the brain, although ␤4GalT-I-deficient mice did not. Here, we investigated the underlying molecular mechanism of the regulation of HNK-1 expression. First, focusing on a major HNK-1 carrier, neural cell adhesion molecule, we found that reduced expression of an N-linked HNK-1 carbohydrate caused by a deficiency of ␤4GalT-II is not likely due to a general loss of the ␤1,4-galactose residue as an acceptor for GlcAT-P. Instead, we demonstrated by co-immunoprecipitation and endoplasmic reticulum-retention analyses using Neuro2a (N2a) cells that ␤4GalT-II physically and specifically associates with GlcAT-P. In addition, we revealed by pulldown assay that Golgi luminal domains of ␤4GalT-II and GlcAT-P are sufficient for the complex to form. With an in vitro assay system, we produced the evidence that the kinetic efficiency k cat /K m of GlcAT-P in the presence of ␤4GalT-II was increased about 2.5-fold compared with that in the absence of ␤4GalT-II. Finally, we showed that co-expression of ␤4GalT-II and GlcAT-P increased HNK-1 expression on various glycoproteins in N2a cells, including neural cell adhesion molecule. These results indicate that the specific enzyme complex of ␤4GalT-II with GlcAT-P plays an important role in the biosynthesis of HNK-1 carbohydrate.

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Section: Discussionmentioning

confidence: 94%

Specific Enzyme Complex of β-1,4-Galactosyltransferase-II and Glucuronyltransferase-P Facilitates Biosynthesis of N-linked Human Natural Killer-1 (HNK-1) Carbohydrate

Kouno

Kizuka

Nakagawa

et al. 2011

Journal of Biological Chemistry

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“…Both b-1,4-GalT-I and -V are thought to be involved in the biosynthesis of Nlinked oligosaccharides (Furukawa and Sato, 1999). It has been shown that b-1,4-GalT-I is the major enzyme that galactosylates N-linked oligosaccharides in the mouse brain (Nakamura et al, 2001). Moreover, our previous study revealed that b-1,4-GalT-I was altered in the injured sciatic nerves of rats (Shen et al, 2002).…”

Section: Introductionmentioning

confidence: 93%

“…The changes of glycosylation that occur on the neuronal surface are thought to be a link with the development and regeneration of the mammalian nervous system (Allendoerfer et al, 1999;Nunome et al, 2008). One study reported that the expression levels of the b1,4-GalT-V transcript increase during mouse brain development after birth, but that the b1,4-GalT-I gene is expressed primarily in the mid-embryonic stages (Liedtke et al, 2001;Nakamura et al, 2001). A related study, however, found that both b-1,4-GalT-I and -V are expressed at low levels in normal sciatic nerve, and play an important role in the regeneration of the injured sciatic nerve, which differed from the expression of b-1,4-GalT-I and -V seen in the central nervous system.…”

Section: Fig 6 (Continued)mentioning

confidence: 99%

“…As we know, b-1,4-GalT-I and -V are involved in the synthesis of the Gal b-1,4-GlcNAc group, and this synthesis of is the basis of HNK-1 carbohydrate and polysialic acid, which are essential for the modification of several nerve-regenerative-associated molecules such as L1 and N-CAM (Furukawa and Sato, 1999;Liedtke et al, 2001;Nakamura et al, 2001). We used lectin-fluorescence staining with RCA-I to further detect the expression changes of the Gal b-1,4-GlcNAc group in microglia and neurons of the cortex and hippocampal regions, which showed that PQQ increased the expression of the Gal b-1,4-GlcNAc group in microglia of the cortex and hippocampal regions compared with that seen in the non-PQQ TBI group.…”

Section: Figmentioning

confidence: 99%

“…Nakamura and colleagues have cloned b-1,4-GalT-I, -II, and -V cDNA using mouse brain and found that both b-1,4-GalT-I and -V have different expression patterns in the development of the brain compared with that of other members of b-1,4-GalTs. During the development of mouse brain, it was found that b-1,4-GalT-I was mainly expressed in the mid-embryonic stage, and that the transcript level of b-1,4-GalT V increased after birth (Zhou et al, 1998;Nakamura et al, 2001). Both b-1,4-GalT-I and -V are thought to be involved in the biosynthesis of Nlinked oligosaccharides (Furukawa and Sato, 1999).…”

Section: Introductionmentioning

confidence: 99%

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The Neuroprotective Effect of Pyrroloquinoline Quinone on Traumatic Brain Injury

Zhang

Liu

Cheng

et al. 2012

Journal of Neurotrauma

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Pyrroloquinoline quinone (PQQ) is a water-soluble, anionic, quinonoid substance that has been established as an essential nutrient in animals. Owing to the inherent properties of PQQ as an antioxidant and redox modulator in various systems, PQQ is expected to be used in pharmacological applications in the near future. Although many recent studies have investigated its neuroprotective effects, the effect of PQQ on traumatic brain injury (TBI) has not been examined. In this study we employed Morris water maze (MWM) training, the results of which showed that PQQ led to improved behavioral performance in post-TBI animals. Considering that many experiments have suggested that b-1,4-galactosyltransferase I (b-1,4-GalT-I) and -V play significant roles in inflammation and the nervous system, in the present study we used Western blot analysis to study the effect of PQQ on the expression of b-1,4-GalT-I and -V. We found apparent expression upregulation of b-1,4-GalT-I and -V after PQQ was systemically administered. Lectin-fluorescent staining with RCA-I also revealed that PQQ contributed to expression upregulation of the galactosidase b-1 (Gal b-1), 4-galactosyltransferase N-acylsphingosine (4-GlcNAc) group in microglia and neurons of the cortex and hippocampal CA2 region. In summary, our experiment established that PQQ may play an important role in recovery post-TBI.

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Expression of β‐1,4‐galactosyltransferase I in rat Schwann cells

Yang

Yan

Cheng

et al. 2009

J of Cellular Biochemistry

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Glycosylation is one of the most important post-translational modifications. It is clear that the single step of beta-1,4-galactosylation is performed by a family of beta-1,4-galactosyltransferases (beta-1,4-GalTs), and that each member of this family may play a distinct role in different tissues and cells. In the present study, real-time PCR revealed that the beta-1,4-GalT I mRNA reached peaks at 2 weeks after sciatic nerve crush and 3 days after sciatic nerve transection. Combined in situ hybridization for beta-1,4-GalT I mRNA and immunohistochemistry for S100 showed that beta-1,4-GalT I mRNAs were mainly located in Schwann cells after sciatic nerve injury. In conclusion, beta-1,4-GalT I might play important roles in Schwann cells during the regeneration and degeneration of the injured sciatic nerve. In other pathology, such as inflammation, we found that LPS administration affected beta-1,4-GalT I mRNA expression in sciatic nerve in a time- and dose-dependent manner, and beta-1,4-GalT I mRNA is expressed mainly in Schwann cells. These results indicated that beta-1,4-GalT I plays an important role in the inflammation reaction induced by intraperitoneal injection of LPS. Similarly, we found that beta-1,4-GalT I in Schwann cells in vitro was affected in a time- and concentration-dependent manner in response to LPS stimulation. All these results suggest that beta-1,4-GalT I play an important role in Schwann cells in vivo and vitro during pathology. In addition, beta-1,4-GalT I production was drastically suppressed by U0126 (ERK inhibitor), SB203580 (p38 inhibitor), or SP600125 (SAPK/JNK inhibitor), which indicated that Schwann cells which regulated beta-1,4-GalT I expression after LPS stimulation were via ERK, SAPK/JNK, and P38 MAP kinase signal pathways.

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Differential gene expression of β‐1,4‐galactosyltransferases I, II and V during mouse brain development

Cited by 46 publications

References 39 publications

Specific Enzyme Complex of β-1,4-Galactosyltransferase-II and Glucuronyltransferase-P Facilitates Biosynthesis of N-linked Human Natural Killer-1 (HNK-1) Carbohydrate

Specific Enzyme Complex of β-1,4-Galactosyltransferase-II and Glucuronyltransferase-P Facilitates Biosynthesis of N-linked Human Natural Killer-1 (HNK-1) Carbohydrate

The Neuroprotective Effect of Pyrroloquinoline Quinone on Traumatic Brain Injury

Expression of β‐1,4‐galactosyltransferase I in rat Schwann cells

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