Ben-Naim Yariv, Falach Lidan, Cohen Yigal
Faculty of Life Sciences, Bar Ilan University, Ramat Gan 5290002, Israel.
Phytopathology. 2018 Jan;108(1):114-123. doi: 10.1094/PHYTO-06-17-0207-R. Epub 2017 Oct 30.
Sweet basil (Ocimum basilicum) is susceptible to downy mildew caused by the oomycete foliar pathogen Peronospora belbahrii. No resistant varieties of sweet basil are commercially available. Here, we report on the transfer of resistance gene Pb1 from the highly resistant tetraploid wild basil O. americanum var. americanum (PI 500945, 2n = 4x = 48) to the tetraploid susceptible O. basilicum 'Sweet basil' (2n = 4x = 48). F1 progeny plants derived from the interspecific hybridization PI 500945 × Sweet basil were resistant, indicating that the gene controlling resistance (Pb1) is dominant, but sterile due to the genetic distance between the parents. Despite their sterility, F1 plants were pollinated with the susceptible parent and 115 first backcross generation to the susceptible parent (BCs1) embryos were rescued in vitro. The emerging BCs1 plants segregated, upon inoculation, 5:1 resistant/susceptible, suggesting that resistance in F1 was controlled by a pair of dominant genes (Pb1A and Pb1A'). Thirty-one partially fertile BCs1 plants were self-pollinated to obtain BCs1-F2 or were backcrossed to Sweet basil to obtain the second backcross generation to the susceptible parent (BCs2). In total, 1 BCs1-F2 and 22 BCs2 progenies were obtained. The BCs1-F2 progeny segregated 35:1 resistant/susceptible, as expected from a tetraploid parent with two dominant resistant genes. The 22 BCs2 progenies segregated 1:1 resistant/susceptible (for a BCs1 parent that carried one dominant gene for resistance) or 5:1 (for a BCs1 parent that carried two dominant genes for resistance) at a ratio of 4:1. The data suggest that a pair of dominant genes (Pb1A and Pb1A') residing on a two homeologous chromosomes is responsible for resistance of PI 500945 against P. belbahrii.
甜罗勒（Ocimum basilicum）易受卵菌叶部病原菌Peronospora belbahrii引起的霜霉病影响。目前市场上没有抗霜霉病的甜罗勒品种。在此，我们报道了将抗性基因Pb1从高度抗性的四倍体野生罗勒O. americanum var. americanum（PI 500945，2n = 4x = 48）转移到四倍体感病的O. basilicum 'Sweet basil'（2n = 4x = 48）中的过程。种间杂交PI 500945×Sweet basil产生的F1后代植株具有抗性，这表明控制抗性的基因（Pb1）是显性的，但由于亲本之间的遗传距离而不育。尽管F1植株不育，但仍用感病亲本对其进行授粉，并在体外拯救了115个回交一代至感病亲本（BCs1）的胚。接种后，新出现的BCs1植株出现分离，抗性/感病比例为5:1，这表明F1中的抗性由一对显性基因（Pb1A和Pb1A'）控制。31株部分可育的BCs1植株进行自花授粉以获得BCs1-F2，或与Sweet basil回交以获得回交二代至感病亲本（BCs2）。总共获得了1个BCs1-F2和22个BCs2后代。BCs1-F2后代的抗性/感病分离比例为35:1，这与具有两个显性抗性基因的四倍体亲本预期相符。对于携带一个抗性显性基因的BCs1亲本，22个BCs2后代的抗性/感病分离比例为1:1；对于携带两个抗性显性基因的BCs1亲本，其分离比例为5:1，比例为4:1。数据表明，位于两条同源染色体上的一对显性基因（Pb1A和Pb1A'）赋予了PI 500945对P. belbahrii的抗性。
