Shanghai Key Laboratory of Plant Molecular Sciences, College of Life Sciences, Shanghai Normal University, Shanghai 200234, China; College of Resources & Environment, Jiujiang University, Jiujiang, Jiangxi 332005, China.
Shanghai Key Laboratory of Plant Molecular Sciences, College of Life Sciences, Shanghai Normal University, Shanghai 200234, China.
Mol Plant. 2021 Dec 6;14(12):2104-2114. doi: 10.1016/j.molp.2021.08.019. Epub 2021 Aug 28.
During anther development, the transformation of the microspore into mature pollen occurs under the protection of first the tetrad wall and later the pollen wall. Mutations in genes involved in this wall transition often lead to microspore rupture and male sterility; some such mutants, such as the reversible male sterile (rvms) mutant, are thermo/photoperiod-sensitive genic male sterile (P/TGMS) lines. Previous studies have shown that slow development is a general mechanism of P/TGMS fertility restoration. In this study, we identified restorer of rvms-2 (res2), which is an allele of QUARTET 3 (QRT3) encoding a polygalacturonase that shows delayed degradation of the tetrad pectin wall. We found that MS188, a tapetum-specific transcription factor essential for pollen wall formation, can activate QRT3 expression for pectin wall degradation, indicating a non-cell-autonomous pathway involved in the regulation of the cell wall transition. Further assays showed that a delay in degradation of the tetrad pectin wall is responsible for the fertility restoration of rvms and other P/TGMS lines, whereas early expression of QRT3 eliminates low temperature restoration of rvms-2 fertility. Taken together, these results suggest a likely cellular mechanism of fertility restoration in P/TGMS lines, that is, slow development during the cell wall transition of P/TGMS microspores may reduce the requirement for their wall protection and thus support their development into functional pollens, leading to restored fertility.
在花粉发育过程中，小孢子向成熟花粉的转化是在四分体壁和花粉壁的保护下进行的。参与这一壁转变的基因发生突变，常导致小孢子破裂和雄性不育；有些突变体，如可逆雄性不育（rvms）突变体，是热/光周期敏感的基因雄性不育（P/TGMS）系。以前的研究表明，发育缓慢是 P/TGMS 育性恢复的一般机制。在这项研究中，我们鉴定了 rvms-2 的恢复基因（res2），它是编码多聚半乳糖醛酸酶的 QUARTET 3（QRT3）的等位基因，表现为四分体果胶壁降解延迟。我们发现，花粉壁形成所必需的绒毡层特异性转录因子 MS188 可以激活 QRT3 的表达，以降解果胶壁，这表明参与调控细胞壁转变的是一个非细胞自主途径。进一步的实验表明，四分体果胶壁降解的延迟是 rvms 和其他 P/TGMS 系育性恢复的原因，而 QRT3 的早期表达消除了 rvms-2 育性对低温恢复的需求。综上所述，这些结果表明 P/TGMS 系育性恢复的一种可能的细胞机制，即在 P/TGMS 小孢子细胞壁转变过程中发育缓慢可能降低其对细胞壁保护的需求，从而支持其发育成有功能的花粉，导致育性恢复。
