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Phi thickenings are specialized secondary walls found in root cortical cells. Despite their widespread occurrence throughout the plant kingdom, these specialized thickenings remain poorly understood. First identified by Van Tieghem in 1871, phi thickenings are a lignified and thickened cell wall band that is deposited inside the primary wall, as a ring around the cells' radial walls. Phi thickenings can, however, display structural variations including a fine, reticulate network of wall thickenings extending laterally from the central lignified band. While phi thickenings have been proposed to mechanically strengthen roots, act as a permeability barrier to modulate solute movement, and regulate fungal interactions, these possibilities remain to be experimentally confirmed. Furthermore, since temporal and spatial development of phi thickenings varies widely between species, thickenings may perform diverse roles in different species. Phi thickenings can be induced by abiotic stresses in different species; they can, for example, be induced by heavy metals in the Zn/Cd hyperaccumulator Thlaspi caerulescens , and in a cultivar-specific manner by water stress in Brassica. This latter observation provides an experimental platform to probe phi thickening function, and to identify genetic pathways responsible for their formation. These pathways might be expected to differ from those involved in secondary wall formation in xylem, since phi thickening deposition in not linked to programmed cell death. [ABSTRACT FROM AUTHOR]

In the Cape Fynbos of South Africa, Psoralea pinnata (L.) plants occur naturally in both wetland and well-drained soils and yet effectively fix N under the two contrasting conditions. In this study, nodule structure and functioning in P. pinnata plants from the two habitats were evaluated using light and transmission electron microscopy (TEM), as well as the N natural abundance technique. The results showed that, structurally, fully developed P. pinnata nodules were spherical in shape with six components (namely, lenticels, periderm, outer cortex, middle cortex, inner cortex, and a central bacteria-infected medulla region). Morphometric analysis revealed 44 and 84 % increase in cell area and volume of wetland nodules compared to those from upland. The percentage area of nodules occupied by the middle cortex in wetland nodules was twice that of upland nodules. As a result, the size of the medulla region in wetland nodules was significantly reduced compared to upland nodules. Additionally, the average area of medulla occupied by intercellular air spaces in wetland nodules was about five times that of upland nodules (about 431 % increase in wetland over upland nodules). TEM data also showed more bacteroids in symbiosomes of upland nodules when compared to wetland nodules. However, isotopic analysis of above-ground plant parts revealed no differences in symbiotic parameters such as N concentration, ∂N and %Ndfa between wetland and upland P. pinnata plants. These results suggest that, under limiting O conditions especially in wetlands, nodules make structural and functional adjustments to meet the O demands of N-fixing bacteroids. [ABSTRACT FROM AUTHOR]

Legume root nodules are induced by N-fixing rhizobium bacteria that are hosted in an intracellular manner. These nodules are formed by reprogramming differentiated root cells. The model legume Medicago truncatula forms indeterminate nodules with a meristem at their apex. This organ grows by the activity of the meristem that adds cells to the different nodule tissues. In Medicago sativa it has been shown that the nodule meristem is derived from the root middle cortex. During nodule initiation, inner cortical cells and pericycle cells are also mitotically activated. However, whether and how these cells contribute to the mature nodule has not been studied. Here, we produce a nodule fate map that precisely describes the origin of the different nodule tissues based on sequential longitudinal sections and on the use of marker genes that allow the distinction of cells originating from different root tissues. We show that nodule meristem originates from the third cortical layer, while several cell layers of the base of the nodule are directly formed from cells of the inner cortical layers, root endodermis and pericycle. The latter two differentiate into the uninfected tissues that are located at the base of the mature nodule, whereas the cells derived from the inner cortical cell layers form about eight cell layers of infected cells. This nodule fate map has then been used to re-analyse several mutant nodule phenotypes. This showed, among other things, that intracellular release of rhizobia in primordium cells and meristem daughter cells are regulated in a different manner. [ABSTRACT FROM AUTHOR]

Endoplasmic reticulum (ER) stress contributes to acute kidney injury induced by several causes. Kidney dysfunction was shown to be influenced by gender differences. In this study we observed differences in the severity of kidney injury between male and female mice in response to tunicamycin, an ER stress agent. Tunicamycin-treated male mice showed a severe decline in kidney function and extensive kidney damage of proximal tubules in the kidney outer cortex (S1 and S2 segments). Interestingly, female tunicamycin-treated mice did not show a decline in kidney function, and their kidneys showed damage localized primarily to proximal tubules in the inner cortex (S3 segment). Protein markers of ER stress, glucose-regulated protein, and X-box binding protein 1 were also more elevated in male mice. Similarly, the induction of apoptosis was higher in tunicamycintreated male mice, as measured by the activation of Bax and caspase-3. Testosterone administered to female mice before tunicamycin resulted in a phenotype similar to male mice with a comparable decline in renal function, tissue morphology, and induction of ER stress markers. We conclude that kidneys of male mice are much more susceptible to ER stress-induced acute kidney injury than those of females. Moreover, this sexual dimorphism could provide an interesting model to study the relation between kidney function and injury to a specific nephron segment. [ABSTRACT FROM AUTHOR]

In the present paper, the modulation of the basolateral membrane (BLM) Na+-ATPase activity of inner cortex from pig kidney by angiotensin II (Ang II) and angiotensin-(1–7) (Ang-(1–7)) was evaluated. Ang II and Ang-(1–7) inhibit the Na+-ATPase activity in a dose-dependent manner (from 10-11 to 10-5 M), with maximal effect obtained at 10-7 M for both peptides. Pharmacological evidences demonstrate that the inhibitory effects of Ang II and Ang-(1–7) are mediated by AT2 receptor: The effect of both polypeptides is completely reversed by 10-8 M PD 123319, a selective AT2 receptor antagonist, but is not affected by either (10-12–10-5 M) losartan or (10-10–10-7 M) A779, selective antagonists for AT1 and AT(1–7) receptors, respectively. The following results suggest that a PTX-insensitive, cholera toxin (CTX)-sensitive G protein/adenosine 3′,5′-cyclic monophosphate (cAMP)/PKA pathway is involved in this process: (1) the inhibitory effect of both peptides is completely reversed by 10-9 M guanosine 5′-O-(2-thiodiphosphate) (GDPβS; an inhibitor of the G protein activity), and mimicked by 10-10 M guanosine 5′-O-(3-thiotriphosphate) (GTPγS; an activator of the G protein activity); (2) the effects of both peptides are mimicked by CTX but are not affected by PTX; (3) Western blot analysis reveals the presence of the Gs protein in the isolated basolateral membrane fraction; (4) (10-10–10-6 M) cAMP has a similar and non-additive effect to Ang II and Ang-(1–7); (5) PKA inhibitory peptide abolishes the effects of Ang II and Ang-(1–7); and (6) both angiotensins stimulate PKA activity. [Copyright &y& Elsevier]

The possibility that cells in the inner cortex of determinate root nodules participate in ureide production from recently fixed N, as do the uninfected (interstitial) cells of the infected central region, has been investigated in soybean ( Glycine max) inoculated as seeds with Bradyrhizobium japonicum. Like the interstitial cells, cells of the three innermost cortical layers produce enlarged peroxisomes and a meshwork of tubular ER during differentiation. These changes are most pronounced in the innermost cortical layer, are successively less so in the 2nd and 3rd layers, and are usually undetectable in more distant layers. Peroxisomes in the inner three layers are stained in the DAB (3,3′-diaminobenzidine) test for uricase (EC 1.7.3.3) activity, indicative of the potential for ureide formation, but peroxisomes in more distant cortical cells are not stained. A nodulespecific uricase also is demonstrable in the inner three cortical layers by immunogold labeling enhanced with silver for visualization in the light microscope. The observations suggest that with respect to ureide production the cells of the inner layers of the cortex are functionally similar to the interstitial cells of the infected region despite the apparent distinctiveness of the two regions anatomically. [ABSTRACT FROM AUTHOR]