C. elegans has two functional peroxidasins (PXN), PXN-1 and PXN-2. PXN-2 is essential to consolidate the extracellular matrix during development and is suggested to interact with PXN-1 antagonistically.
pxn-1 is involved in neuronal development and possibly maintenance; therefore, we investigated the relationship between
pxn-1 and
pxn-2 in neuronal development and in aging. During neuronal development, defects caused by
pxn-1 overexpression were suppressed by overexpression of both
pxn-1 and
pxn-2. In neuronal aging process,
pxn-1 mutants showed less age-related neuronal defects, such as neuronal outgrowth, neuronal wavy processes, and enhanced short-term memory performance. In addition,
pxn-2 overexpressing animals retained an intact neuronal morphology when compared with age-matched controls. Consistent with these results, overexpression of both
pxn-1 and
pxn-2 restored the severe neuronal defects present with
pxn-1 overexpression. These results implied that there is a negative relationship between
pxn-1 and
pxn-2 via
pxn-1 regulating
pxn-2. Therefore,
pxn-1 may function in neuronal development and age-related neuronal maintenance through
pxn-2.