A katanin-like protein regulates normal cell wall biosynthesis and cell elongation

Fibers are one of the mechanical tissues that provide structural support to the plant body. To understand how the normal mechanical strength of fibers is regulated, we isolated an Arabidopsis fragile fiber (fra2) mutant defec tive in the mechanical strength of interfascicular fibers in the infloresce nce stems. Anatomical and chemical analyses showed that the fra2 mutation c aused a reduction in fiber cell length and wall thickness, a decrease in ce llulose and hemicellulose contents, and an increase in lignin condensation, indicating that the fragile fiber phenotype of fra2 is a result of alterat ions in fiber cell elongation and cell wail biosynthesis, In addition to th e effects on fibers, the fra2 mutation resulted in a remarkable reduction i n cell length and an increase in cell width in all organs, which led to a g lobal alteration in plant morphology. The FRA2 gene was shown to encode a p rotein with high similarity to katanin (hence FRA2 was renamed AtKTN1), a p rotein shown to be involved in regulating microtubule disassembly by severi ng microtubules. Consistent with the putative function of AtKTN1 as a micro tubule-severing protein, immunolocalization demonstrated that the fra2 muta tion caused delays in the disappearance of perinuclear microtubule array an d in the establishment of transverse cortical microtubule array in interpha se and elongating cells. Together, these results suggest that AtKTN1, a kat anin-like protein, is essential not only for normal cell wall biosynthesis and cell elongation in fiber cells but also for cell expansion in all organ s.