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MKK7 deficiency in mature neurons impairs parental behavior in mice
Genes to Cells ( IF 1.3 ) Pub Date : 2020-10-23 , DOI: 10.1111/gtc.12816 Tadashi Shin 1 , Yuichi Hiraoka 2 , Tokiwa Yamasaki 1, 3 , Jamey D Marth 4 , Josef M Penninger 5, 6 , Masami Kanai-Azuma 7 , Kohichi Tanaka 2 , Satoshi Kofuji 1 , Hiroshi Nishina 1
Genes to Cells ( IF 1.3 ) Pub Date : 2020-10-23 , DOI: 10.1111/gtc.12816 Tadashi Shin 1 , Yuichi Hiraoka 2 , Tokiwa Yamasaki 1, 3 , Jamey D Marth 4 , Josef M Penninger 5, 6 , Masami Kanai-Azuma 7 , Kohichi Tanaka 2 , Satoshi Kofuji 1 , Hiroshi Nishina 1
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c‐Jun N‐terminal kinases (JNKs) are constitutively activated in mammalian brains and are indispensable for their development and neural functions. MKK7 is an upstream activator of all JNKs. However, whether the common JNK signaling pathway regulates the brain's control of social behavior remains unclear. Here, we show that female mice in which Mkk7 is deleted specifically in mature neurons (Mkk7flox/floxSyn‐Cre mice) give birth to a normal number of pups but fail to raise them due to a defect in pup retrieval. To explore the mechanism underlying this abnormality, we performed comprehensive behavioral tests. Mkk7flox/floxSyn‐Cre mice showed normal locomotor functions and cognitive ability but exhibited depression‐like behavior. cDNA microarray analysis of mutant brain revealed an altered gene expression pattern. Quantitative RT‐PCR analysis demonstrated that mRNA expression levels of genes related to neural signaling pathways and a calcium channel were significantly different from controls. In addition, loss of neural MKK7 had unexpected regulatory effects on gene expression patterns in oligodendrocytes. These findings indicate that MKK7 has an important role in regulating the gene expression patterns responsible for promoting normal social behavior and staving off depression.
中文翻译：
成熟神经元中的MKK7缺乏会损害小鼠的父母行为
c-Jun N-末端激酶（JNKs）在哺乳动物的大脑中被组成性激活，对于它们的发育和神经功能必不可少。MKK7是所有JNK的上游激活剂。但是，目前尚不清楚JNK信号通路是否能调节大脑对社交行为的控制。在这里，我们显示出在成熟神经元中特异删除了Mkk7的雌性小鼠（Mkk7 flox / flox Syn-Cre小鼠）可生出正常数量的幼崽，但由于幼崽取回缺陷而无法饲养它们。为了探索这种异常的潜在机制，我们进行了全面的行为测试。Mkk7 Flox / Flox Syn‐Cre小鼠表现出正常的运动功能和认知能力，但表现出抑郁样行为。突变脑的cDNA微阵列分析揭示了基因表达模式的改变。定量RT‐PCR分析表明，与神经信号通路和钙通道相关的基因的mRNA表达水平与对照显着不同。此外，神经MKK7的丢失对少突胶质细胞的基因表达模式具有意想不到的调节作用。这些发现表明，MKK7在调节负责促进正常社会行为和预防抑郁的基因表达模式中具有重要作用。
更新日期：2020-10-23
中文翻译：
成熟神经元中的MKK7缺乏会损害小鼠的父母行为
c-Jun N-末端激酶（JNKs）在哺乳动物的大脑中被组成性激活，对于它们的发育和神经功能必不可少。MKK7是所有JNK的上游激活剂。但是，目前尚不清楚JNK信号通路是否能调节大脑对社交行为的控制。在这里，我们显示出在成熟神经元中特异删除了Mkk7的雌性小鼠（Mkk7 flox / flox Syn-Cre小鼠）可生出正常数量的幼崽，但由于幼崽取回缺陷而无法饲养它们。为了探索这种异常的潜在机制，我们进行了全面的行为测试。Mkk7 Flox / Flox Syn‐Cre小鼠表现出正常的运动功能和认知能力，但表现出抑郁样行为。突变脑的cDNA微阵列分析揭示了基因表达模式的改变。定量RT‐PCR分析表明，与神经信号通路和钙通道相关的基因的mRNA表达水平与对照显着不同。此外，神经MKK7的丢失对少突胶质细胞的基因表达模式具有意想不到的调节作用。这些发现表明，MKK7在调节负责促进正常社会行为和预防抑郁的基因表达模式中具有重要作用。
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