[Effects of topographic factors on leaf traits of apricot in the Loess Plateau, Northwest China]. / åœ°å½¢å› å­å¯¹é»„åœŸé«˜åŽŸå±±æå¶ç‰‡åŠŸèƒ½æ€§çŠ¶çš„å½±å“.

As important topographic factors, slope aspect and gradient affect plant growth and leaf functional traits by regulating the combination of water and heat. Exploring the response of leaf functional traits to topographic factors is helpful for understanding plant adaptation strategies. We investigated the effects of sunny slope (including half sunny slope) and shady slope (including half shady slope) and three slope gradient (15°-20°, 21°-25°, and 26°-30°) on the leaf functional traits of apricot (Prunus armeniaca L.), the main afforestation tree species on the Loess Plateau. The results showed that: 1) Slope aspect and gradient exerted significant effects on all functional traits. Except leaf water content (LWC), other leaf functional traits were not affected by the interaction of slope aspect and gradient. 2) The leaf area (LA) under the sunny slope was equivalent to that under the shady slope. Leaf dry matter content (LDMC) and LWC (0.27 g·g-1 and 67.0%, respectively) were significantly higher under the shady slope than under the sunny slope (0.24 g·g-1 and 59.6%, respectively), while specific leaf area (SLA) (163.05 cm2·g-1) was significantly lower under the former than under the latter (183.72 cm2·g-1). 3) At different slope gradients, SLA and LA reached a maximum value at 15°-20° (184.04 cm2·g-1) and 26°-30° (21.14 cm2), respectively. 4) Except no difference in soil water content (Θ) between 15°-20° and 26°-30°, it differed significantly between two slope aspects and among other slope gradients. The Θ was one of the main factors causing the differences in functional traits, especially in the 0-10 cm soil layer. 5) SLA was negatively correlated with LWC and LDW and positively correlated with LA. LDW was positively correlated with LWC and negatively correlated with LA. Θ was positively correlated with LWC but not with other leaf functional traits.

ELP3 Acetyltransferase is phosphorylated and regulated by the oncogenic anaplastic lymphoma kinase (ALK).

Protein lysine acetylation is one of the major posttranslational modifications (PTMs) with several thousands of proteins identified to be acetylated in mammalian tissues. Mechanistic studies have revealed important functions of acetylation in the regulation of protein function. Much less is known on how the acetyltransferases themselves are regulated. In the current study, we discover that the Elongator protein 3 (ELP3) acetyltransferase is modified by tyrosine phosphorylation. We demonstrate that the anaplastic lymphoma kinase (ALK) is the major tyrosine kinase responsible for ELP3 tyrosine phosphorylation. ELP3 is phosphorylated in tumor cells expressing oncogenic NPM-ALK fusion protein. We further identify Tyr202 as the major ALK phosphorylation site in ELP3. Importantly, the introduction of Y202 phosphorylation mutant ELP3 into ALK-positive tumor cells reduced cell growth and impaired gene expression. Collectively, our study reveals a novel regulatory mechanism for ELP3, provides an example that acetyltransferase itself can be regulated by PTM, and suggests a potential target for ALK-positive cancer therapies.

Elevational variations of leaf stochiometry in Leontopodium leontopodioides on the Qinghai-Tibetan Plateau, China.

Topography has major impacts on the trade-off of plant survival strategies. Exploring the differential pattern of leaf ecological stoichiometry along the elevation gradient contributes to a better understanding of plant's response to environmental changes and its ecological adaptability. We investigated leaf C, N, and P concentrations and stoichiometric ratios of Leontopodium leontopodioides at three elevations, including from 4400 m to 4700 m, from 4701 m to 5000 m, and from 5001 m to 5300 m, on the northeastern margin of the Qinghai-Tibetan Plateau in China. The results showed that the concentrations of leaf C, N, and P of L. leontopodioides were 405.36 g·kg-1, 18.42 g·kg-1 and 0.94 g·kg-1, respectively. Leaf C/N, C/P, and N/P were 22.67, 467.61 and 20.30, respectively. The concentrations of leaf N and P of L. leontopodioides consistently increased with the increases of elevation. The coefficient of variations for leaf C, N and P concentrations and ratios of L. leontopodioides were all less than 30%, with an order of P (30%) > C/P (29%) > C/N (18%) > N (17%) > N/P (15%) > C (3%). The growth of L. leontopodioides on the Qinghai-Tibetan Plateau was mainly limited by P availability.

[Effects of grassland management on soil nutrients and their spatial distribution on the Qinghai-Tibetan Plateau, China]. / é’è—é«˜åŽŸè‰åœ°ç®¡ç†æ–¹å¼å¯¹åœŸå£¤å »åˆ†åŠå ¶ç©ºé—´åˆ†å¸ƒçš„å½±å“.

After grasslands were contracted to individual households on the Qinghai-Tibetan Pla-teau, two grassland management patterns were formed, i.e., the single-household management pattern (SMP) and the multi-household management pattern (MMP). The soil nutrients and their spatial distributions under those two patterns were compared in the Nagchu Prefecture of Tibet. The results showed that the soil organic carbon, total nitrogen, and total phosphorus under the MMP (84.31, 6.87 and 0.59 g·kg-1) were all significantly higher than those under the SMP (73.57, 6.07 and 0.54 g·kg-1). On the vertical dimension, the variation coefficient of soil total phosphorous between 0-15 cm layer and 15-30 cm layer under SMP had no significant difference, while that of soil pH, soil organic carbon and total nitrogen in 15-30 cm layer were all higher than 0-15 cm layer under both patterns. On the horizontal dimension, the variation coefficients of soil organic carbon and total nitrogen under SMP were significantly higher than those under MMP, with the estimated values for the former being 25.7% and 23.5%, and for the latter being 19.3% and 18.6%, respectively. Compared with the MMP, the uneven distribution of nutrients could easily lead to soil nutrient loss under the SMP.

Thromboxane A2 Activates YAP/TAZ Protein to Induce Vascular Smooth Muscle Cell Proliferation and Migration.

The thromboxane A2 receptor (TP) has been implicated in restenosis after vascular injury, which induces vascular smooth muscle cell (VSMC) migration and proliferation. However, the mechanism for this process is largely unknown. In this study, we report that TP signaling induces VSMC migration and proliferation through activating YAP/TAZ, two major downstream effectors of the Hippo signaling pathway. The TP-specific agonists [1S-[1α,2α(Z),3ß(1E,3S*),4 α]]-7-[3-[3-hydroxy-4-(4-iodophenoxy)-1-butenyl]-7-oxabicyclo[2.2.1]hept-2-yl]-5-heptenoic acid (I-BOP) and 9,11-dideoxy-9α,11α-methanoepoxy-prosta-5Z,13E-dien-1-oic acid (U-46619) induce YAP/TAZ activation in multiple cell lines, including VSMCs. YAP/TAZ activation induced by I-BOP is blocked by knockout of the receptor TP or knockdown of the downstream G proteins Gα12/13 Moreover, Rho inhibition or actin cytoskeleton disruption prevents I-BOP-induced YAP/TAZ activation. Importantly, TP activation promotes DNA synthesis and cell migration in VSMCs in a manner dependent on YAP/TAZ. Taken together, thromboxane A2 signaling activates YAP/TAZ to promote VSMC migration and proliferation, indicating YAP/TAZ as potential therapeutic targets for cardiovascular diseases.

NOTCH-induced aldehyde dehydrogenase 1A1 deacetylation promotes breast cancer stem cells.

High aldehyde dehydrogenase (ALDH) activity is a marker commonly used to isolate stem cells, particularly breast cancer stem cells (CSCs). Here, we determined that ALDH1A1 activity is inhibited by acetylation of lysine 353 (K353) and that acetyltransferase P300/CBP-associated factor (PCAF) and deacetylase sirtuin 2 (SIRT2) are responsible for regulating the acetylation state of ALDH1A1 K353. Evaluation of breast carcinoma tissues from patients revealed that cells with high ALDH1 activity have low ALDH1A1 acetylation and are capable of self-renewal. Acetylation of ALDH1A1 inhibited both the stem cell population and self-renewal properties in breast cancer. Moreover, NOTCH signaling activated ALDH1A1 through the induction of SIRT2, leading to ALDH1A1 deacetylation and enzymatic activation to promote breast CSCs. In breast cancer xenograft models, replacement of endogenous ALDH1A1 with an acetylation mimetic mutant inhibited tumorigenesis and tumor growth. Together, the results from our study reveal a function and mechanism of ALDH1A1 acetylation in regulating breast CSCs.