HYDRAULIC SIGNALS FROM THE ROOTS AND RAPID CELL-WALL HARDENING IN GROWING MAIZE (ZEA-MAYS L) LEAVES ARE PRIMARY RESPONSES TO POLYETHYLENE GLYCOL-INDUCED WATER DEFICITS
O. Chazen et Pm. Neumann, HYDRAULIC SIGNALS FROM THE ROOTS AND RAPID CELL-WALL HARDENING IN GROWING MAIZE (ZEA-MAYS L) LEAVES ARE PRIMARY RESPONSES TO POLYETHYLENE GLYCOL-INDUCED WATER DEFICITS, Plant physiology, 104(4), 1994, pp. 1385-1392
We investigated mechanisms involved in inhibition of maize (Zea mays L
.) leaf-elongation growth following addition of nonpenetrating osmolyt
e to the root medium. The elongation rate of the first true leaf remai
ned inhibited for 4 h after addition of polyethylene glycol 6000 (PEG;
-0.5 MPa water potential), despite progressive osmotic adjustment in
the growing leaf tissues. Thus, inhibition of leaf growth did not appe
ar to be directly related to loss of leaf capacity to maintain osmotic
potential gradients. Comparative cell-wall-extension capacities of im
mature (still expanding) leaf tissues were measured by creep extensiom
etry using whole plants. Reductions in irreversible (plastic) extensio
n capacity (i.e. wall hardening) were detected minutes and hours after
addition of PEG to the roots, by both in vivo and in vitro assay. The
onset of the wall-hardening response could be detected by in vitro as
say only 2 min after addition of PEG. Thus, initiation of wall hardeni
ng appeared to precede transcription-regulated responses. The inhibiti
on of both leaf growth and wall-extension capacity was reversed by rem
oval of PEG after 4 h. Moreover, wall hardening could be induced by ot
her osmolytes (mannitol, NaCl). Thus, the leaf responses did not appea
r to be related to any specific (toxic) effect of PEC. We conclude tha
t hardening of leaf cell walls is a primary event in the chain of grow
th regulatory responses to PEG-induced water deficits in maize. The si
gnaling processes by which PEG, which is not expected to penetrate roo
t cell walls or membranes, might cause cell-wall hardening in relative
ly distant leaves was also investigated. Plants with live or killed ro
ots were exposed to PEG. The killed roots were presumed to be unable t
o produce hormonal or electrical signals in response to addition of PE
C; however, inhibition of leaf elongation and hardening of leaf cell w
alls were detected with both live and killed roots. Thus, neither horm
onal signaling nor signaling via induced changes in surface electrical
potential were necessary, and hydraulic signals appeared to generate
the leaf responses.