Predicting mating patterns from pollination syndromes: the case of "sapromyiophily" in Tacca chantrieri (Taccaceae)

Tacca, a genus of tropical herbs, possesses near black flowers, conspicuous involucral bracts and whisker-like filiform bracteoles. These features have been assumed to function as a "deceit syndrome" in which reproductive structures resemble decaying organic material attracting flies that facilitate cross-pollination (sapromyiophily). We investigated pollination and mating in Tacca chantrieri populations from SW China to evaluate this assumption. Contrary to this expectation, populations were highly selfing. Pollinator visitation was infrequent and bagged flowers set abundant seed. Pollen loads on stigmas indicated autonomous self-pollination, some of which occurred prior to flower opening. The seed set of inflorescences with bracts and bracteoles removed was not significantly different from unmanipulated inflorescences, suggesting that these structures play a limited role in pollinator attraction, at least at our study sites. Pollen : ovule ratios averaged 49, a value expected in a highly selfing species. Selfing rates estimated in four populations using allozyme markers averaged 0.86 (range 0.76-0.94), thus corroborating this inference. Our results indicate that despite considerable investment in extravagant display, populations of T. chantrieri are highly selfing. We propose several hypotheses to resolve this paradox and argue that future studies of pollination syndromes would benefit by investigation of both pollination and mating biology.     

Molar enamel thickness in the chacma baboon, Papio ursinus (Kerr 1792)

Modern humans exhibit increasing relative enamel thickness from M1 to M3. Some biomechanical (basic lever) models predict that the more distal molars in humans encounter higher occlusal forces, and it has been postulated that this provides a functional explanation for the observed gradient in relative enamel thickness. However, constrained three-dimensional models and experimental observations suggest that there is a reduction in bite force potential from M1 to M3, which would be consistent with the tendency for humans to reduce the size of the distal molars. In this regard, it has been postulated that the distal increase in enamel thickness is a consequence of crown size reduction; thus, it is unnecessary to invoke functional scenarios to explain this phenomenon. We assess these competing proposals by examining relative enamel thickness in a catarrhine primate (Papio ursinus) that exhibits crown size increase from M1 to M3. The molar row of P. ursinus is positioned relatively far forward of the temporomandibular joint, which results in the baboon being able to exert relatively greater muscle forces during posterior biting in comparison to modern humans. Thus, a significant distalward gradient of increasing enamel thickness would be expected in P. ursinus according to the hypothesis that posits it to be functionally related to bite force. The present study reveals no significant difference in relative enamel thickness along the molar row in P. ursinus. This finding lends support to the notion that the relatively thicker enamel of human distal molars is related primarily to their reduction in size. This carries potential implications for the interpretation of enamel thickness in phylogenetic reconstructions: the relatively thick molar enamel shared by modern humans and some of our fossil relatives may not be strictly homologous, in that it may result from different underlying developmental mechanisms.     

Mechanisms governing the level of susceptibility of erythrocyte membranes to secretory phospholipase A2

Although cell membranes normally resist the hydrolytic action of secretory phospholipase A(2) (sPLA(2)), they become susceptible during apoptosis or after cellular trauma. Experimentally, susceptibility to the enzyme can be induced by loading cells with calcium. In human erythrocytes, the ability of the calcium ionophore to cause susceptibility depends on temperature, occurring best above approximately 35 degrees C. Considerable evidence from experiments with artificial bilayers suggests that hydrolysis of membrane lipids requires two steps. First, the enzyme adsorbs to the membrane surface, and second, a phospholipid diffuses from the membrane into the active site of the adsorbed enzyme. Analysis of kinetic experiments suggested that this mechanism can explain the action of sPLA(2) on erythrocyte membranes and that temperature and calcium loading promote the second step. This conclusion was further supported by binding experiments and assessment of membrane lipid packing. The adsorption of fluorescent-labeled sPLA(2) was insensitive to either temperature or ionophore treatment. In contrast, the fluorescence of merocyanine 540, a probe sensitive to lipid packing, was affected by both. Lipid packing decreased modestly as temperature was raised from 20 to 60 degrees C. Calcium loading enhanced packing at temperatures in the low end of this range, but greatly reduced packing at higher temperatures. This result was corroborated by measurements of the rate of extraction of a fluorescent phosphatidylcholine analog from erythrocyte membranes. Furthermore, drugs known to inhibit susceptibility in erythrocytes also prevented the increase in phospholipid extraction rate. These results argue that the two-step model applies to biological as well as artificial membranes and that a limiting step in the hydrolysis of erythrocyte membranes is the ability of phospholipids to migrate into the active site of adsorbed enzyme.     

Treadmill running produces both positive and negative physiological adaptations in Sprague-Dawley rats

Exercise training produces a vast array of physiological adaptations, ranging from changes in metabolism to muscle mitochondrial biogenesis. Researchers studying the physiological effects of exercise often use animal models that employ forced exercise regimens that include aversive motivation, which could activate the stress response. This study examined the effect of forced treadmill running (8 wk) on several physiological systems that are sensitive to training and stress. Forced treadmill running produced both positive and negative physiological adaptations. Indicative of positive training adaptations, exercised male Sprague-Dawley rats had a decrease in body weight gain and an increase in muscle citrate synthase activity compared with sedentary controls. In contrast, treadmill running also resulted in the potentially negative adaptations of adrenal hypertrophy, thymic involution, decreased serum corticosteroid binding globulin, elevated lymphocyte nitrite concentrations, suppressed lymphocyte proliferation, and suppressed antigen-specific IgM. Such alterations in neuroendocrine tissues and immune responses are commonly associated with chronic stress. Thus treadmill running produces both positive training adaptations and potentially negative adaptations that are indicative of chronic stress. Researchers employing forced activity need to be aware that this type of exercise procedure also produces physiological adaptations indicative of chronic stress and that these changes could potentially impact other measures of interest.     

Plasma apolipoprotein L concentrations correlate with plasma triglycerides and cholesterol levels in normolipidemic, hyperlipidemic, and diabetic subjects

Apolipoprotein L is a newly recognized component of human plasma lipoproteins. Mainly associated with apoA-I-containing lipoproteins, it is a marker of distinct HDL subpopulations. In an effort to gain inference as to its as yet unknown function, we studied biological determinants of apoL levels in human plasma. The distribution of apoL in normal subjects is asymmetric, with marked skewing toward higher values. No difference was found in apoL concentrations between males and females, but we observed an elevation of apoL in primary hypercholesterolemia (10.1 vs. 8.5 microgram/mL in control), in endogenous hypertriglyceridemia (13.8 microgram/mL, P < 0.001), combined hyperlipidemia phenotype (18.7 g/mL, P < 0.0001), and in patients with type II diabetes (16.2 microgram/mL, P < 0.02) who were hyperlipidemic. Significant positive correlations were observed between apoL and the log of plasma triglycerides in normolipidemia (0.446, P < 0.0001), endogenous hypertriglyceridemia (0.435, P < 0.01), primary hypercholesterolemia (0.66, P < 0.02), combined hyperlipidemia (0.396, P < 0.04), hypo-alphalipoproteinemia (0.701, P < 0.005), and type II diabetes with hyperlipidemia (0.602, P < 0. 01). Apolipoprotein L levels were also correlated with total cholesterol in normolipidemia (0.257, P < 0.004), endogenous hypertriglyceridemia (0.446, P = 0.001), and non-insulin-dependent diabetes mellitus (NIDDM) (0.548, P < 0.02). No significant correlation was found between apoL and body mass index, age, sex, HDL-cholesterol or fasting glucose and glycohemoglobin levels. ApoL levels in plasma of patients with primary cholesteryl ester transfer protein deficiency significantly increased (7.1 +/- 0.5 vs. 5.47 +/- 0.27, P < 0.006).     

Interaction of the tumor suppressor PTEN/MMAC with a PDZ domain of MAGI3, a novel membrane-associated guanylate kinase

PTEN/MMAC is a phosphatase that is mutated in multiple human tumors. PTEN/MMAC dephosphorylates 3-phosphorylated phosphatidylinositol phosphates that activate AKT/protein kinase B (PKB) kinase activity. AKT/PKB is implicated in the inhibition of apoptosis, and cell lines and tumors with mutated PTEN/MMAC show increased AKT/PKB kinase activity and resistance to apoptosis. PTEN/MMAC contains a PDZ domain-binding site, and we show here that the phosphatase binds to a PDZ domain of membrane-associated guanylate kinase with inverted orientation (MAGI) 3, a novel inverted membrane-associated guanylate kinase that localizes to epithelial cell tight junctions. Importantly, MAGI3 and PTEN/MMAC cooperate to modulate the kinase activity of AKT/PKB. These data suggest that MAGI3 allows for the juxtaposition of PTEN/MMAC to phospholipid signaling pathways involved with cell survival.     

ErbB2 is necessary for induction of carcinoma cell invasion by ErbB family receptor tyrosine kinases

The epidermal growth factor (EGF) family of tyrosine kinase receptors (ErbB1, -2, -3, and -4) and their ligands are involved in cell differentiation, proliferation, migration, and carcinogenesis. However, it has proven difficult to link a given ErbB receptor to a specific biological process since most cells express multiple ErbB members that heterodimerize, leading to receptor cross-activation. In this study, we utilize carcinoma cells depleted of ErbB2, but not other ErbB receptor members, to specifically examine the role of ErbB2 in carcinoma cell migration and invasion. Cells stimulated with EGF-related peptides show increased invasion of the extracellular matrix, whereas cells devoid of functional ErbB2 receptors do not. ErbB2 facilitates cell invasion through extracellular regulated kinase (ERK) activation and coupling of the adaptor proteins, p130CAS and c-CrkII, which regulate the actin-myosin cytoskeleton of migratory cells. Overexpression of ErbB2 in cells devoid of other ErbB receptor members is sufficient to promote ERK activation and CAS/Crk coupling, leading to cell migration. Thus, ErbB2 serves as a critical component that couples ErbB receptor tyrosine kinases to the migration/invasion machinery of carcinoma cells.