Researchers at Rice University have found that the protein PEX11 not only helps peroxisomes divide but also regulates their size during early plant development. In Arabidopsis seedlings, PEX11 mutants developed abnormally large peroxisomes lacking internal vesicles that normally curb growth. The mechanism appears conserved across species, as yeast Pex11 restored normal function in plant mutants.
During the seed-to-seedling stage, Arabidopsis plants rely on peroxisomes to break down stored fatty acids for energy before photosynthesis begins. These organelles enlarge temporarily then shrink, a process now linked to PEX11, a protein long known for aiding peroxisome division. Rice University researchers, led by Bonnie Bartel, published their findings in Nature Communications, revealing PEX11's additional role in size control. Nathan Tharp, the study's first author, noted peroxisomes' relevance to human diseases and bioengineering but their difficulty in study. Bartel highlighted Arabidopsis's large cells, making peroxisomes visible under light microscopes, especially during fatty acid reliance when they peak in size before contracting. To probe PEX11, produced by five genes, Tharp employed advanced CRISPR techniques to disrupt specific combinations. Single-gene knockouts had minimal impact, but targeted multi-gene disruptions proved lethal or revealed defects. In viable mutants lacking certain PEX11 genes, peroxisomes expanded as expected but failed to shrink, sometimes spanning entire cells. These giants lacked intralumenal vesicles, small compartments that form during fatty acid processing and pinch off membrane pieces to limit growth. Tharp explained, 'The vesicles taking pieces of membrane as they form may help control the peroxisome's growth.' Remarkably, introducing yeast Pex11 into mutant plants normalized peroxisome size, indicating a conserved mechanism. Bartel said this suggests applicability to human cells and bioengineering applications.
