Complete deletion of Slc52a2 causes embryonic lethality in mice

Congyun Jin, Yoshihiro Matsui, Atsushi Yonezawa, Satoshi Imai, Takashi Ogihara, Kotaro Itohara, Shunsaku Nakagawa, Takayuki Nakagawa, Kazuo Matsubara

研究成果: Article査読

2 被引用数 (Scopus)


Riboflavin (vitamin B2) plays an important role in cellular growth and function. Riboflavin transporter 2 (RFVT2) is widely expressed in several tissues, especially in the brain and salivary glands, and plays an important role in the tissue disruption of riboflavin. During the last 10 years, mutations in SLC52A2 have been documented in patients with a rare neurological disorder known as Brown–Vialetto–Van Laere syndrome. However, no suitable animal model of this disease has been reported. Here, we aimed to clarify the physiological role of RFVT2 using Slc52a2-mutant mice. The appearance, body weight, and plasma riboflavin concentration of Slc52a2 heterozygous mutant (Slc52a2+/−) mice were similar to those of wild-type (WT) mice. However, intercrossing between Slc52a2+/− mice failed to generate Slc52a2 homozygous mutant (Slc52a2−/−) mice. This suggested that Slc52a2 gene deficiency results in early embryonic lethality. Our findings suggested that RFVT2 is essential for growth and development, and its deletion may influence embryonic survival.

ジャーナルBiological and Pharmaceutical Bulletin
出版ステータスPublished - 2021 2月 1

ASJC Scopus subject areas

  • 薬理学
  • 薬科学


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