Loss of partitioning-defective-3/isotype-specific interacting protein (Par-3/ASIP) in the elongating spermatid of RA175 (IGSF4A/SynCAM)-deficient mice
Loss of partitioning-defective-3/isotype-specific interacting protein (Par-3/ASIP) in the elongating spermatid of RA175 (IGSF4A/SynCAM)-deficient mice
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DOI：
10.2353/ajpath.2007.070261
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发表时间：
2007-12-01
影响因子：
6
通讯作者：
Momoi, Takashi
中科院分区：
文献类型：
--
作者：
Fujita, Eriko;Tanabe, Yuko;Momoi, Takashi
IGSF4a/RA175/SynCAM (RA175) 和连接粘附分子 (Jams) 是免疫球蛋白超家族的成员，其 C 末端具有 PDZ 结合结构域。 Ra175 (Ra175(-/-)) 缺乏和 jam-C 缺乏 (Jam-C-/-) 会导致精子细胞分化缺陷，即少弱畸形精子症。 Ra175(-/-) 延长精子细胞；无法进一步成熟，而 Jam-C-/- 圆形精子细胞失去细胞极性，并且大多数 Jam-C-/- 拉长精子细胞完全丧失。 RA175 和 Jam-C 在精子细胞中似乎具有相似但不同的功能作用。差异化。在这里，我们表明，具有 PDZ 结构域的细胞极性蛋白 Par-3（果酱的结合伴侣）是睾丸中 RA175 细胞质区域的相关蛋白之一。 Par-3 和 Jam-C 在伸长和伸长的精子细胞中与 RA175 部分共定位；它们的分布与野生型中伸长精子细胞头部背侧区域尖端上的 RA175 重叠（步骤 9 至 12）。在Ra175(-/-)-伸长精子细胞中，Par-3缺失，Jam-C缺失或异常定位。 RA175 通过与 Par-3 相互作用与 Jam-C 形成三元复合物。 Ra175(-/-)伸长精子细胞中三元复合物的缺乏可能导致特化粘附结构的缺陷，导致少弱畸形精子症。
IGSF4a/RA175/SynCAM (RA175) and junctional adhesion molecules (Jams) are members of the immunoglobulin superfamily with a PDZ-binding domain at their C termini. Deficiency of Ra175 (Ra175(-/-)) as well as jam-C deficiency (Jam-C-/-) causes the defect of the spermatid differentiation, oligo-astheno-teratozoospermia. Ra175(-/-) elongating spermatids; fail to mature further, whereas Jam-C-/- round spermatids lose cell polarity, and most of Jam-C-/- elongated spermatids are completely lost. RA175 and Jam-C seem to have similar but distinct functional roles during spermatid. differentiation. Here we show that the cell polarity protein Par-3 with PDZ domains, a binding partner of jams, is one of the associated proteins of the cytoplasmic region of RA175 in testis. Par-3 and Jam-C are partly co-localized with RA175 in the elongating and elongated spermatids; their distributions overlapped with that of RA175 on the tips of the dorsal region of the head of the elongating spermatid (steps 9 to 12) in the wild type. In the Ra175(-/-)-elongating spermatid, Par-3 was absent, and Jam-C was absent or abnormally localized. The RA175 formed a ternary complex with Jam-C via interaction with Par-3. The lack of the ternary complex in the Ra175(-/-) elongating spermatid may cause the defect of the specialized adhesion structures, resulting in the oligo-astheno-teratozoospermia.