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首页> 外文期刊>Journal of Experimental Botany >Altered tapetal PCD and pollen wall development in the Arabidopsis ms1 mutant
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Altered tapetal PCD and pollen wall development in the Arabidopsis ms1 mutant

机译：拟南芥ms1突变体中绒毛PCD和花粉壁发育的改变

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摘要

The Arabidopsis male sterility1 mutation results in mature anthers that are devoid of pollen. Meiosis and early development progress normally; however, after microspore release, the microspore cytoplasm and tapetum become abnormally granular and vacuolated, and degeneration occurs. Pollen wall development is seriously affected; primexine formation within the callose wall appears to occur normally, however, once the callose is degraded, abnormal deposits of electrodense material are detected which result in irregular spike-shaped structures, rather than the characteristic rod-like shape of the wild-type bacula. The internal intine wall is also reduced compared with wild type. TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling) staining and ultrastructural analysis have indicated that programmed cell death (PCD) occurs in the wild-type tapetum after microspore mitosis I. However, no signs of PCD are seen in the ms1 tapetum, where large autophagic vacuoles and mitochondrial swelling suggest that necrotic-based breakdown of the tapetum is occurring in the ms1 mutant rather than the normal, regulated PCD process. After the formation of the large, autophagic vacuole in the tapetum, TUNEL staining is detected in the mutant microspores, indicating that they may go through a PCD-based breakdown as a secondary consequence of the observed tapetal aberrations. Based on these observations, two possible roles for MS1 can be hypothesized; MS1 may function by modifying the transcription of tapetal-specific genes implicated in pollen wall development, which then regulate pollen wall material secretion and in turn wall development and tapetal PCD. Alternatively, the MS1 gene may control tapetal development by directly regulating tapetal PCD and breakdown.
机译：拟南芥雄性不育1突变导致没有花粉的成熟花药。减数分裂和早期发育正常；然而，释放小孢子后，小孢子的细胞质和绒毡层变得异常颗粒状和空泡化，并发生变性。花粉壁的发育受到严重影响；愈伤组织壁内的primxine形成似乎正常发生，但是，一旦愈伤组织降解，就会检测到电极蛋白物质的异常沉积，这会导致形成不规则的穗状结构，而不是野生型小肠的杆状特征。与野生型相比，内部intine壁也减少了。 TUNEL（末端脱氧核苷酸转移酶介导的dUTP缺口末端标记）染色和超微结构分析表明，小孢子有丝分裂I发生后，野生型绒毡层发生了程序性细胞死亡（PCD）。但是，在ms1绒毡层中未见PCD的迹象，其中大量的自噬空泡和线粒体肿胀表明绒毛基于坏死的分解发生在ms1突变体中，而不是正常的，受调控的PCD过程。在绒毡层中形成较大的自噬泡之后，在突变的小孢子中检测到TUNEL染色，表明它们可能由于观察到的绒毡层畸变而经历了基于PCD的分解。基于这些观察，可以假设MS1有两个可能的作用： MS1可能通过修饰与花粉壁发育有关的绒毡层特异性基因的转录而起作用，然后调节花粉壁物质的分泌，进而调节花粉壁物质的分泌和绒毡层PCD。另外，MS1基因可以通过直接调节绒毛PCD和分解来控制绒毛的发育。

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