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雌性小鼠缺乏岩藻糖变位酶表现出雄性性行为。

Male-like sexual behavior of female mouse lacking fucose mutarotase.

机构信息

Department of Biological Sciences, Korea Advanced Institute of Science and Technology, 335 Gwahangno, Yuseong-Gu, Daejon 305-701, Korea.

出版信息

BMC Genet. 2010 Jul 7;11:62. doi: 10.1186/1471-2156-11-62.

Abstract

BACKGROUND

Mutarotases are recently characterized family of enzymes that are involved in the anomeric conversions of monosaccharides. The mammalian fucose mutarotase (FucM) was reported in cultured cells to facilitate fucose utilization and incorporation into protein by glycosylation. However, the role of this enzyme in animal has not been elucidated.

RESULTS

We generated a mutant mouse specifically lacking the fucose mutarotase (FucM) gene. The FucM knockout mice displayed an abnormal sexual receptivity with a drastic reduction in lordosis score, although the animals were fertile due to a rare and forced intromission by a typical male. We examined the anteroventral periventricular nucleus (AVPv) of the preoptic region in brain and found that the mutant females showed a reduction in tyrosine hydoxylase positive neurons compared to that of a normal female. Furthermore, the mutant females exhibited a masculine behavior, such as mounting to a normal female partner as well as showing a preference to female urine. We found a reduction of fucosylated serum alpha-fetoprotein (AFP) in a mutant embryo relative to that of a wild-type embryo.

CONCLUSIONS

The observation that FucM-/- female mouse exhibits a phenotypic similarity to a wild-type male in terms of its sexual behavior appears to be due to the neurodevelopmental changes in preoptic area of mutant brain resembling a wild-type male. Since the previous studies indicate that AFP plays a role in titrating estradiol that are required to consolidate sexual preference of female mice, we speculate that the reduced level of AFP in FucM-/- mouse, presumably resulting from the reduced fucosylation, is responsible for the male-like sexual behavior observed in the FucM knock-out mouse.

摘要

背景

变位酶是一类最近被描述的酶,参与单糖的端基转换。哺乳动物岩藻糖变位酶(FucM)在培养细胞中被报道能促进岩藻糖的利用,并通过糖基化掺入蛋白质。然而,该酶在动物中的作用尚未阐明。

结果

我们生成了一种特异性缺乏岩藻糖变位酶(FucM)基因的突变小鼠。FucM 敲除小鼠表现出异常的性接受能力,发情评分明显降低,尽管由于典型雄性的罕见和强制插入,这些动物是可育的。我们检查了大脑前脑区腹前核(AVPv),发现突变雌性与正常雌性相比,酪氨酸羟化酶阳性神经元减少。此外,突变雌性表现出雄性行为,如向正常雌性伴侣交配,以及对雌性尿液表现出偏好。我们发现突变胚胎中结合珠蛋白血清 α-胎蛋白(AFP)的岩藻糖基化水平相对野生型胚胎降低。

结论

FucM-/-雌性小鼠在性行为方面表现出与野生型雄性相似的表型,这似乎是由于突变大脑前脑区的神经发育变化类似于野生型雄性。由于先前的研究表明 AFP 在调节雌二醇方面发挥作用,而雌二醇是巩固雌性小鼠性偏好所必需的,因此我们推测 FucM-/-小鼠中 AFP 水平降低,可能是由于岩藻糖基化减少,导致观察到的雄性样性行为。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f94f/2912782/070a549f1176/1471-2156-11-62-1.jpg

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