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擬南芥TRANSPORTIN 1互作基因的遺傳篩選

發(fā)布時(shí)間:2018-05-16 19:03

  本文選題:TRANSPORTIN + 1。 參考:《蘭州大學(xué)》2017年碩士論文


【摘要】:TRANSPORTIN 1(TRN1)是擬南芥Importinβ家族17個(gè)成員之一。其酵母及哺乳動(dòng)物細(xì)胞中同源蛋白的主要功能是對(duì)目的蛋白的入核轉(zhuǎn)運(yùn),從而影響了眾多生物學(xué)過(guò)程。另外,越來(lái)越多的證據(jù)表明,它也能夠通過(guò)一些非核質(zhì)轉(zhuǎn)運(yùn)的方式發(fā)揮作用,比如通過(guò)促進(jìn)microRNAs和ARGONOUTE 1的相互結(jié)合來(lái)正調(diào)控前者的活性,但并不涉及它們的核質(zhì)分布調(diào)控。為了尋找TRN1更多的遺傳互作基因,我們首先對(duì)其突變體進(jìn)行了表型及等位分析,發(fā)現(xiàn)它是莖尖頂端分生組織(shoot apical meristem,SAM)正常發(fā)育和維持的必需基因。在此基礎(chǔ)之上,我們對(duì)其弱突變體sic1進(jìn)行了基于轉(zhuǎn)基因激活標(biāo)簽(activation tagging)技術(shù)的二次誘變,篩選到了一些抑制子和增強(qiáng)子。對(duì)其中一個(gè)抑制子B639的進(jìn)一步分析表明,KAKTUS(KAK)基因的表達(dá)水平缺陷可能是導(dǎo)致其表型的原因。因此,我們利用TRN1和KAK的等位突變體構(gòu)建了更多組合的雙突變體,并對(duì)其表型進(jìn)行了相關(guān)分析,確定了這兩個(gè)基因的遺傳互作關(guān)系。本研究的結(jié)果對(duì)進(jìn)一步研究它們的分子作用機(jī)制,尤其是在調(diào)控SAM活性過(guò)程中的作用,奠定了堅(jiān)實(shí)的基礎(chǔ)。
[Abstract]:TRANSPORTIN 1 (TRN 1) is one of 17 members of Importin 尾 family in Arabidopsis thaliana. The main function of homologous proteins in yeast and mammalian cells is to transport the target proteins into the nucleus, thus affecting many biological processes. In addition, there is growing evidence that it can also play a role in non-nuclear transport, for example by promoting the interaction of microRNAs and ARGONOUTE 1 to positively regulate the activity of the former, but not their nuclear and cytoplasmic distribution. In order to search for more genetic interaction genes of TRN1, we first analyzed the phenotype and alleles of its mutant, and found that it is an essential gene for the normal development and maintenance of shoot apical meristemin. On the basis of this, the weak mutant sic1 was screened by secondary mutagenesis based on transgene activation tagging technique, and some suppressor and enhancer were screened. Further analysis of one of the suppressor B639 showed that the deficiency in the expression level of kakTUSKK) gene may be the cause of its phenotype. Therefore, we constructed more combinations of double mutants using allelic mutants of TRN1 and KAK, analyzed their phenotypes and determined the genetic interaction between the two genes. The results of this study laid a solid foundation for further study of their molecular mechanism, especially in the process of regulating the activity of SAM.
【學(xué)位授予單位】:蘭州大學(xué)
【學(xué)位級(jí)別】:碩士
【學(xué)位授予年份】:2017
【分類號(hào)】:Q943.2

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