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The Gene ANTHER DEHISCENCE REPRESSOR (ADR) Controls Male Fertility by Suppressing the ROS Accumulation and Anther Cell Wall Thickening in Arabidopsis. | LitMetric

AI Article Synopsis

  • Male sterility in plants can be triggered by various factors like hormonal changes, stress, and gene mutations, with the ANTHER DEHISCENCE REPRESSOR (ADR) gene playing a key role in regulating it in Arabidopsis.
  • The study found that ADR is highly active in young flower buds but less so in mature flowers, and its ectopic expression leads to male sterility due to issues with anther dehiscence (the process by which pollen is released).
  • The male sterility is linked to reduced reactive oxygen species (ROS) accumulation and decreased expression of key genes (NST1 and NST2) necessary for the anther's structural integrity, with hydrogen peroxide treatment able to reverse

Article Abstract

Male sterility in plants is caused by various stimuli such as hormone changes, stress, cytoplasmic alterations and nuclear gene mutations. The gene ANTHER DEHISCENCE REPRESSOR (ADR), which is involved in regulating male sterility in Arabidopsis, was functionally analyzed in this study. In ADR::GUS flowers, strong GUS activity was detected in the anthers of young flower buds but was low in mature flowers. ADR + GFP fusion proteins, which can be modified by N-myristoylation, were targeted to peroxisomes. Ectopic expression of ADR in transgenic Arabidopsis plants resulted in male sterility due to anther indehiscence. The defect in anther dehiscence in 35S::ADR flowers is due to the reduction of ROS accumulation, alteration of the secondary thickening in the anther endothecium and suppression of the expression of NST1 and NST2, which are required for anther dehiscence through regulation of secondary wall thickening in anther endothecial cells. This defect could be rescued by external application of hydrogen peroxide (HO). These results demonstrated that ADR must be N-myristoylated and targeted to the peroxisome during the early stages of flower development to negatively regulate anther dehiscence by suppressing ROS accumulation and NST1/NST2 expression.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6434047PMC
http://dx.doi.org/10.1038/s41598-019-41382-zDOI Listing

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