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The historical beginning of understanding the importance of water to life started with the Ionic Philosophers (from the Ionic Sea), who began to think that physiology (referring to nature, from the ancient Greek physis ¼ nature; logos ¼ talk) could explain life better than theology (referring to god, from the ancient Greek theos ¼ god; logos ¼ talk). Among these, Talete (624–547 BC) is credited with the observation that he ‘‘principle of nature is water,’’ and all life begins with water. In this essay, we explain how water moves through plants and is used for growth by recounting the history of ideas, observations, and experimentation that form our present basis of understanding of plant water homeostasis. We briefly summarize the history of approaches and discoveries that have identified the growing collection of genes that control altered growth and/or altered water use properties of plants during osmotic mediated stresses, with the exception of freezing stress. These genes, which have often been identified by forward genetic mutation screens, impact one or more of several mechanisms controlling water absorption, movement, and use. A better understanding of the basis of water homeostasis should be a useful tool in the arsenal of molecular geneticists, and increased awareness of the utility of genetics to understand adaptation to osmotic stress should be a great benefit to physiologists.

LRRK2 mutations can cause familial and sporadic Parkinson's disease (PD) with Lewy-body pathology at post-mortem. Studies of olfaction in LRRK2 are sparse and incongruent. We applied a previously validated translation of the 16 item smell identification test from Sniffin' Sticks (SS-16) to 14 parkinsonian carriers of heterozygous G2019S LRRK2 mutation and compared with 106 PD patients and 118 healthy controls. The mean SS-16 score in LRRK2 was higher than in PD (p < 0.001, 95% CI for beta = -4.7 to -1.7) and lower than in controls (p = 0.007, 95% CI for beta = +0.6 to +3.6). In the LRRK2 group, subjects with low scores had significantly more dyskinesia. They also had younger age of onset, longer disease duration, and reported less frequently a family history of PD, but none of these other differences reached significance. Odor identification is diminished in LRRK2 parkinsonism but not to the same extent as in idiopathic PD. (C) 2010 Movement Disorder Society

A hyper-osmotically sensitive mutant of Arabidopsis thaliana, designated hos3-1 (high expression of osmotically responsive genes), was identified based on its hyper-luminescence of RD29A:LUC promoter fusion plants upon treatment with NaCl and ABA. These responses implicate the disrupted gene as a direct or indirect negative regulator of the RD29A stress-responsive pathway. By sequencing the flanking regions of the T-DNA borders, it was determined that the disrupted gene is at locus At4g36830, annotated as encoding a putative protein with high homology to CIG30 (ELO2/FEN1). CIG30 has been implicated in synthesis of very long chain fatty acids (VLCFA), which are essential precursors for sphingolipids and ceramides. Altered stress responses characteristic of ABA-hypersensitivity, including reduced root growth inhibition and reduced germination with ABA treatment and reduced water loss from leaves, were exhibited by allelic hos3-1 and hos3-2 mutants. The hos3-2 mutant is partially suppressed in its transcript abundance and is inherited as a recessive trait. Further, the HOS3 ORF under the control of the 35SCaMV promoter restored wild-type NaCl- and ABA-root growth sensitivity as well as RD29A:LUC luminescence in mutant plants. We also show here that the HOS3 wild-type gene functionally complements the sensitivity of elo2 and elo3 yeast mutants to monensin. Furthermore, both hos3-1 and hos3-2 alleles shared increased sensitivity to the herbicide Metolachlor, which inhibits acyl chain elongation in synthesis of VLCFA, and HOS3 functionally complemented both elo2 and elo3 and restored levels of VLCFA. Together, these data establish that HOS3 inhibits ABA-mediated stress responses and implicate the VLCFA pathway and products as control points for several aspects of abiotic stress signaling and responses. The results also provide support for a role of ceramide in the control of stomatal behavior.

In recent years the study of the functional biology of salinity tolerance in plants has largely focused on six major areas of research: ion homeostasis, water homeostasis, osmolyte production, ROS scavenging, growth regulatory processes, and signal transduction. Genetic engineering and mutation analyses have both significantly contributed to advance our understanding of the fundamental biology underlying salt stress adaptation. Many biochemical and metabolic components of salinity tolerance have been thoroughly described and directly and/or indirectly implicated in salt stress adaptation at cellular level. In contrast, morphological and anatomical features that also may have important functions during whole plant stress adaptation have been overlooked. Mutants with altered responses to salinity in agriculturally important species are increasingly, and represent an important resource for plant physiologists and agronomists that are interested in understanding salinity tolerance at a whole plant level. The results obtained so far suggest that a greater connection between molecular genetic and physiological analyses would greatly benefit the functional assessment of plant salt stress tolerance.