Drosophila female germline stem cells undergo mitosis without nuclear breakdown

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Disentangling the link between leaf photosynthesis and turgor in fruit growth

Despite the importance of understanding plant growth, the mechanisms underlying how plant and fruit growth declines during drought remain poorly understood. Specifically, it remains unresolved whether carbon or water factors are responsible for limiting growth as drought progresses. We examine questions regarding the relative importance of water and carbon to fruit growth depending on the water deficit level and the fruit growth stage by measuring fruit diameter, leaf photosynthesis, and a proxy of cell turgor in olive (Olea europaea). Flow cytometry was also applied to determine the fruit cell division stage. We found that photosynthesis and turgor were related to fruit growth; specifically, the relative importance of photosynthesis was higher during periods of more intense cell division, while turgor had higher relative importance in periods where cell division comes close to ceasing and fruit growth is dependent mainly on cell expansion. This pattern was found regardless of the water deficit level, although turgor and growth ceased at more similar values of leaf water potential than photosynthesis. Cell division occurred even when fruit growth seemed to stop under water deficit conditions, which likely helped fruits to grow disproportionately when trees were hydrated again, compensating for periods with low turgor. As a result, the final fruit size was not severely penalized. We conclude that carbon and water processes are able to explain fruit growth, with importance placed on the combination of cell division and expansion. However, the major limitation to growth is turgor, which adds evidence to the sink limitation hypothesis.     

Respiratory enzymes in muscle: Interaction between environmental temperature, nutrition and growth

1. 1.In young pigs living at 35 or 10°C on a high or low energy intake, respiratory enzyme activities in longissimus dorsi muscle were greater both in the cold and on low intake. The elevated activities in the cold were unlikely to be related entirely to shivering since they were also found in muscle from the diaphragm.

2. 2.In a second study, pigs were kept close to thermal neutrality (26°C) on different levels of food intake and for different periods of time. For all animals, as body weight increased there was a decline in respiratory enzyme activity and the number of dark fibres in skeletal muscle. For those of the same weight, but different age and food intake, there was no difference in enzyme activity or number of dark fibres per unit area.

3. 3.At least part of the difference in respiratory enzyme activities related to energy intake must therefore be due to differences in body size. However, size is not the sole determinant of enzyme activity in skeletal muscle, since in animals of similar size those living at 10°C have greater enzyme activities than those at 35°C.

Accuracy of body mass estimates of formalin-preserved fish – a review

This paper highlights possible effects of physical and chemical mechanisms of formalin fixation and preservation on biological tissue and reviews the consequent potential inaccuracies on estimates of body mass of small fishes fixed and preserved in formalin. Twenty-six papers including 65 independent experiments with 35 species which examine effects of formalin on body mass estimates on small fishes are included. The effect of the formalin on the specimens depends on the salinity of the water used to dilute the commercial formalin (usually 1:9 formalin: water) before being used to fixate and preserve fish. Mean wet body mass of the specimens from the studies using seawater or fresh water diluted formalin deceases by 13% and increases by 7%, respectively, from before to after being immersed in formalin. The same trend is found with condition factor in the few papers that report this parameter. Body length decreases on average by c. 2% in fixated and preserved fish regardless of whether the formalin is diluted in seawater or fresh water.     

VEGF-C attenuates renal damage in salt-sensitive hypertension

Salt-sensitive hypertension is a major risk factor for renal impairment leading to chronic kidney disease. High-salt diet leads to hypertonic skin interstitial volume retention enhancing the activation of the tonicity-responsive enhancer-binding protein (TonEBP) within macrophages leading to vascular endothelial growth factor C (VEGF-C) secretion and NOS3 modulation. This promotes skin lymphangiogenesis and blood pressure regulation. Whether VEGF-C administration enhances renal and skin lymphangiogenesis and attenuates renal damage in salt-sensitive hypertension remains to be elucidated. Hypertension was induced in BALB/c mice by a high-salt diet. VEGF-C was administered subcutaneously to high-salt-treated mice as well as control animals. Analyses of kidney injury, inflammation, fibrosis, and biochemical markers were performed in vivo. VEGF-C reduced plasma inflammatory markers in salt-treated mice. In addition, VEGF-C exhibited a renal anti-inflammatory effect with the induction of macrophage M2 phenotype, followed by reductions in interstitial fibrosis. Antioxidant enzymes within the kidney as well as urinary RNA/DNA damage markers were all revelatory of abolished oxidative stress under VEGF-C. Furthermore, VEGF-C decreased the urinary albumin/creatinine ratio and blood pressure as well as glomerular and tubular damages. These improvements were associated with enhanced TonEBP, NOS3, and lymphangiogenesis within the kidney and skin. Our data show that VEGF-C administration plays a major role in preserving renal histology and reducing blood pressure. VEGF-C might constitute an interesting potential therapeutic target for improving renal remodeling in salt-sensitive hypertension.     

Minireview: Metabolic control of the reproductive physiology: Insights from genetic mouse models

This article is part of a Special Issue Energy Balance.     

Schwannoma-Derived Growth Factor Interacts with the Epidermal Growth Factor Receptor

Abstract: Schwannoma-derived growth factor (SDGF) is a potent mitogen and neuronal differentiation factor. Because of its relationship to epidermal growth factor (EGF) and the heregulins, it was asked if SDGF interacts with the EGF receptor or HER2/neu. SDGF binds to and causes the phosphorylation on tyrosine of the EGF receptor but not HER2/neu.     

Resistance training-induced muscle hypertrophy is mediated by TGF-β1-Smad signaling pathway in male Wistar rats

The TGF-β1-Smad pathway is a well-known negative regulator of muscle growth; however, its potential role in resistance training-induced muscle hypertrophy is not clear. The present study proposed to determine whether and how this pathway may be involved in resistance training-induced muscle hypertrophy. Skeletal muscle samples were collected from the control, trained (RT), control + SB431542 (CI_TGF), and trained + SB431542 (RTI_TGF) animals following 3, 5, and 8 weeks of resistance training. Inhibition of the TGF-β1-Smad pathway by SB431542 augmented muscle satellite cells activation, upregulated Akt/mTOR/S6K1 pathway, and attenuated FOXO1 and FOXO3a expression in the CI_TGF group (all p < .01), thereby causing significant muscle hypertrophy in animals from the CI_TGF. Resistance training significantly decreased muscle TGF-β1 expression and Smad3 (P-Smad3^S423/425) phosphorylation at COOH-terminal residues, augmented Smad2 (P-Smad2-L^S245/250/255) and Smad3 (P-Smad3-L^Ser208) phosphorylation levels at linker sites (all p < .01), and led to a muscle hypertrophy which was unaffected by SB431542, suggesting that the TGF-β1-Smad signaling pathway is involved in resistance training-induced muscle hypertrophy. The effects of inhibiting the TGF-β1-Smad signaling pathway were not additive to the resistance training effects on FOXO1 and FOXO3a expression, muscle satellite cells activation, and the Akt/mTOR/S6K1 pathway. Resistance training effect of satellite cell differentiation was independent of the TGF-β1-Smad signaling pathway. These results suggested that the effect of the TGF-β1-Smad signaling pathway on resistance training-induced muscle hypertrophy can be attributed mainly to its diminished inhibitory effects on satellite cell activation and protein synthesis. Suppressed P-Smad3^S423/425 and enhanced P-Smad2-L^S245/250/255 and P-Smad3-L^Ser208 are the molecular mechanisms that link the TGF-β1-Smad signaling pathway to resistance training-induced muscle hypertrophy.