MYC（8q24）基因断裂探针

MYC（8q24）基因断裂探针

 广州健仑生物科技​有限公司 

本司长期供应尼古丁（可替宁）检测试剂盒，其主要品牌包括美国NovaBios、广州健仑、广州创仑等进口产品，国产产品，试剂盒的实验方法是胶体金方法。

我司还有很多荧光原位杂交系列检测试剂盒以及各种FISH基因探针和染色体探针等，。

MYC（8q24）基因断裂探针

   本试剂盒主要用于MYC（8q24）基因断裂的检测，里面包括即用型杂交液和DAPI复染剂。
本试剂盒仅供科研使用。

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【公司名称】 广州健仑生物科技有限公司
【】    杨永汉 

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【腾讯 】
【公司地址】 广州清华科技园创新基地番禺石楼镇创启路63号二期2幢101-3室

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生殖细胞负责遗传信息的时代传递，那么基因组的完整性对于生殖细胞至关重要。而在真核生物精细胞中，有许多外来侵入的转座子、逆转座子等移动型遗传元件。这些自私的遗传元件在染色体不同位点间跳跃，造成基因突变和基因组损伤。在生殖细胞中，转座子的跳跃可能会导致不育。PiRNA/Piwi能够高效的阻止转座子等元件对基因组的损伤。研究发现，piRNA起源于反转座子、重复序列等区域，与Piwi蛋白形成piRNA/Piwi机器，沉默转座子、反转座子等。此外，piRNA还可以发挥类似于siRNA的功能，参与调控生殖细胞中编码基因的表达。

方法：

研究人员发现无精子症患者体内Piwi（Hiwi）生殖突变会阻止其泛素化和降解。为了了解其中的作用机制，研究人员构建了Piwi（Miwi）突变敲入小鼠模型，证明了这种遗传缺陷直接导致了男性不育症。具体来说，研究人员发现MIWI能以一种对立于Piwi作用RNA（piRNA）的方式，与组蛋白泛素连接酶RNF8结合，并在晚期精子细胞的细胞质中稳定螯合RNF8，从而导致精子异常，引起组蛋白滞留，形态异常和活性严重受损，而这可以通过RNF8-N阻断精子细胞中RNF8-MIWI的相互作用，逆转功能。

结果1：

研究人员筛查了413例临床无精、弱精症患者Piwi基因上控制Piwi蛋白泛素化修饰降解的关键元件D-box，发现有3例病人在此元件中存在杂合性基因突变，且发现此类突变可来源于基因自发突变，也可从母亲遗传获得。为鉴定此类突变是否是造成这些患者发生无精/少弱精的原因，研究人员将其中的一组突变条件型敲入小鼠Piwi基因，在小鼠模型中研究此类突变对精子发生的作用。他们发现， Piwi D-box杂合突变小鼠均出现雄性不育，精子表型也与患者*。深入研究发现，Miwi D-box杂合突变小鼠精子发生阻滞在延长型精子细胞发育阶段，尽管能产生少量精子，但精子形态异常、细胞核结构疏松、无活力。

结果2：

机制研究揭示， PIWI蛋白具有将RNF8“扣留”于细胞核外的功能。正常小鼠体内PIWI蛋白会在精子发育后期被自然降解，RNF8进入细胞核内开启“组蛋白-鱼精蛋白转换”，帮助精子发育完成。而Piwi蛋白突变导致其在后期不能被正常代谢，大量RNF8因此被“扣留”在细胞核外，鱼精蛋白与组蛋白交换受阻，zui终造成精子发育受阻。将RNF8-N端导入突变小鼠的精子细胞后，可有效阻断Piwi基因蛋白产物对RNF8的“扣留”，恢复精子的正常形态及游动能力，提示该策略对临床治疗此类无精、弱精症具有重要理论参考价值。

Reproductive cells are responsible for the transmission of genetic information, then the integrity of the genome is crucial to the germ cells. In eukaryote, there are many intruded transposons, reverse transposons, and other genetic elements. These selfish genetic elements jump between chromosomal locations, causing gene mutations and genome damage. In the germ cells, the leaping of the transposon may lead to infertility. PiRNA/Piwi can effectively prevent the damage to the genome by the components of the transposon. It is found that piRNA originates in the retrotransposon, repeat sequence and other regions, and forms the piRNA/Piwi machine with the Piwi protein, silencing the transposon, and the retrotransposon. In addition, piRNA can also play a role similar to siRNA and participate in the regulation of the expression of encoded genes in the germ cells.

Method：

The researchers found that Piwi (Hiwi) mutagenesis in the body of azoospermia prevents its ubiquitination and degradation. In order to understand the mechanism, the researchers constructed a Piwi (Miwi) in mouse model of mutation, proved the genetic defects directly lead to male infertility. Specifically, the researchers found that MIWI in a Piwi RNA (piRNA) in the way of combination with histone RNF8 ubiquitin ligase, and stable chelate RNF8 in advanced sperm cell cytoplasm, resulting in abnormal sperm, cause protein retention, abnormal morphology and activity severely damaged, this can be done by RNF8-N blocking the interaction of RNF8-MIWI in sperm cells, reverse function.

Results 1:

The key element of D-box researchers screened 413 cases of azoospermia and weak sperm Piwi in patients with Piwi gene controlling protein ubiquitination and degradation, discovered the existence of heterozygous mutations in 3 patients in this element, and found that these mutations can be derived from spontaneous mutation gene can be inherited from his mother. For the identification of such mutations is the cause of azoospermia / little weak sperm occurred in these patients, the researchers will be a group of mutant type Piwi gene knock in mouse condition which, in a mouse model of such mutations on spermatogenesis function. They found that the Piwi D-box heterozygous mutant mice were male sterility, and the sperm phenotype was also consistent with the patient. Further studies showed that Miwi D-box heterozygous mutant mice had spermatogenesis arrest at the extended stage of spermatogenesis, although they produced a small amount of sperm, but the sperm morphology was abnormal, the nuclear structure was loose and inactive.

Results 2:

The mechanism studies have revealed that PIWI protein has the function of "withholding" RNF8 outside the nucleus. In normal mice, PIWI protein will be degraded naturally in the late stage of sperm development. RNF8 will enter into the nucleus and start the histone protamine transformation to help sperm development. However, the mutation of Piwi protein causes it to not be metabolize in the late stage. A large number of RNF8 is therefore "arrested" outside the nucleus. The exchange of protamine and histone is hindered, resulting in the development of sperm is blocked. After introducing the RNF8-N terminal into the spermatozoa of the mutant mice, it can effectively block the retention of Piwi protein products to RNF8 and restore the normal morphology and swimming ability of the sperm, suggesting that this strategy has important theoretical reference value for the clinical treatment of such azoospermia and asthenospermia.