Relationship between leaf physiologic traits and canopy color indices during the leaf expansion period in an oak forest

© The Author(s), 2015. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in Ecosphere 6, no. 12 (2015): 1-9, doi:10.1890/ES14-00452.1.Plant phenology has a significant impact on the forest ecosystem carbon balance. Detecting plant phenology by capturing the time-series canopy images through digital camera has become popular in recent years. However, the relationship between color indices derived from camera images and plant physiological characters are elusive during the growing season in temperate ecosystems. We collected continuous images of forest canopy, leaf size, leaf area index (LAI) and leaf chlorophyll measured by a soil plant analysis development (SPAD) analyzer in a northern subtropical oak forest in China. Our results show that (1) the spring peak of color indices, Gcc (Green Chromatic Coordinates) and ExG (Excess Green), was 18 days earlier than the 90% maximum SPAD value; (2) the 90% maximum SPAD value coincided with the change point of Gcc and ExG immediately after their spring peak; and (3) the spring curves of Gcc and ExG before their peaks were highly synchronous with the expansion of leaf size and the development of LAI value. We suggest it needs to be adjusted if camera-derived Gcc or ExG is used as a proxy of chlorophyll or gross primary productivity, and images observation should be complemented with field phenological and physiological information to interpret the physiological meaning of leaf seasonality.This research was funded by the Priority Academic Program Development of Jiangsu Higher Education Institutions in the Discipline of Environmental Science and Engineering at Nanjing Forest University, Changjiang River Delta Urban Forest Ecosystem Research of CFERN (to H. Hu) and Brown University Seed Funds for International Research Projects on the Environment (to J. Tang)

Tulp1 deficiency causes early-onset retinal degeneration through affecting ciliogenesis and activating ferroptosis in zebrafish

Mutations in TUB-like protein 1 (TULP1) are associated with severe early-onset retinal degeneration in humans. However, the pathogenesis remains largely unknown. There are two homologous genes of TULP1 in zebrafish, namely tulp1a and tulp1b. Here, we generated the single knockout (tulp1a(−/−) and tulp1b(−/−)) and double knockout (tulp1-dKO) models in zebrafish. Knockout of tulp1a resulted in the mislocalization of UV cone opsins and the degeneration of UV cones specifically, while knockout of tulp1b resulted in mislocalization of rod opsins and rod-cone degeneration. In the tulp1-dKO zebrafish, mislocalization of opsins was present in all types of photoreceptors, and severe degeneration was observed at a very early age, mimicking the clinical manifestations of TULP1 patients. Photoreceptor cilium length was significantly reduced in the tulp1-dKO retinas. RNA-seq analysis showed that the expression of tektin2 (tekt2), a ciliary and flagellar microtubule structural component, was downregulated in the tulp1-dKO zebrafish. Dual-luciferase reporter assay suggested that Tulp1a and Tulp1b transcriptionally activate the promoter of tekt2. In addition, ferroptosis might be activated in the tulp1-dKO zebrafish, as suggested by the up-regulation of genes related to the ferroptosis pathway, the shrinkage of mitochondria, reduction or disappearance of mitochondria cristae, and the iron and lipid droplet deposition in the retina of tulp1-dKO zebrafish. In conclusion, our study establishes an appropriate zebrafish model for TULP1-associated retinal degeneration and proposes that loss of TULP1 causes defects in cilia structure and opsin trafficking through the downregulation of tekt2, which further increases the death of photoreceptors via ferroptosis. These findings offer insight into the pathogenesis and clinical treatment of early-onset retinal degeneration

Structural transition, electric transport, and electronic structures in the compressed trilayer nickelate La4Ni3O10

Atomic structure and electronic band structure are fundamental properties for understanding the mechanism of superconductivity. Motivated by the discovery of pressure-induced high-temperature superconductivity at 80 K in the bilayer Ruddlesden-Popper nickelate La3Ni2O7, the atomic structure and electronic band structure of the trilayer nickelate La4Ni3O10 under pressure up to 44.3 GPa are investigated. A structural transition from the monoclinic P21/a space group to the tetragonal I4/mmm around 12.6-13.4 GPa is identified, accompanying with a drop of resistance below 7 K. Density functional theory calculations suggest that the bonding state of Ni 3dz2 orbital rises and crosses the Fermi level at high pressures, which may give rise to possible superconductivity observed in resistance under pressure in La4Ni3O10. The trilayer nickelate La4Ni3O10 shows some similarities with the bilayer La3Ni2O7 and has unique properties, providing a new platform to investigate the underlying mechanism of superconductivity in nickelates.Comment: 19 pages, 4 figure

Single crystal growth and superconductivity in RbNi2_2Se2_2

We report the synthesis and characterization of RbNi$_2$Se$_2$, an analog of the iron chalcogenide superconductor Rb$_x$Fe$_2$Se$_2$, via transport, angle resolved photoemission spectroscopy, and density functional theory calculations. A superconducting transition at $T_{c}$ = 1.20 K is identified. In normal state, RbNi$_2$Se$_2$ shows paramagnetic and Fermi liquid behaviors. A large Sommerfeld coefficient yields a heavy effective electron mass of $m^{*}\approx6m_{e}$. In the superconducting state, zero-field electronic specific-heat data $C_{es}$ can be described by a two-gap BCS model, indicating that RbNi$_2$Se$_2$ is a multi-gap superconductor. Our density functional theory calculations and angle resolved photoemission spectroscopy measurements demonstrate that RbNi$_2$Se$_2$ exhibits relatively weak correlations and multi-band characteristics, consistent with the multi-gap superconductivity.Comment: 7 pages, 4 figure

The splicing factor DHX38 enables retinal development through safeguarding genome integrity

DEAH-Box Helicase 38 (DHX38) is a pre-mRNA splicing factor and also a disease-causing gene of autosomal recessive retinitis pigmentosa (arRP). The role of DHX38 in the development and maintenance of the retina remains largely unknown. In this study, by using the dhx38 knockout zebrafish model, wedemonstrated that Dhx38 deficiency causes severe differentiation defects and apoptosis of retinal progenitor cells (RPCs) through disrupted mitosis and increased DNA damage. Furthermore, we found a significant accumulation of R-loops in the dhx38-deficient RPCs and human cell lines. Finally, we found that DNA replication stress is the prerequisite for R-loop-induced DNA damage in the DHX38 knockdown cells. Taken together, our study demonstrates a necessary role of DHX38 in the development of retina and reveals a DHX38/R-loop/replication stress/DNA damage regulatory axis that is relatively independent of the known functions of DHX38 in mitosis control

RHOA-regulated IGFBP2 promotes invasion and drives progression of BCR-ABL1 chronic myeloid leukemia

The Philadelphia 9;22 chromosome translocation has two common isoforms that are preferentially associated with distinct subtypes of leukemia. The p210 variant is the hallmark of chronic myeloid leukemia (CML) whereas p190 is frequently associated with B-cell acute lymphoblastic leukemia. The only sequence difference between the two isoforms is the guanidine exchange factor domain. This guanidine exchange factor is reported to activate RHO family GTPases in response to diverse extracellular stimuli. It is not clear whether and, if so, how RHOA contributes to progression of p210 CML. Here we show that knockout of RHOA in the K562 and KU812, p210-expressing cell lines leads to suppression of leukemogenesis in animal models in vivo. RNA-sequencing analysis of the mock control and null cells demonstrated a distinct change in the gene expression profile as a result of RHOA deletion, with significant downregulation of genes involved in cell activation and cell adhesion. Cellular analysis revealed that RHOA knockout leads to impaired cell adhesion and migration and, most importantly, the homing ability of leukemia cells to the bone marrow, which may be responsible for the attenuated leukemia progression. We also identified IGFBP2 as an important downstream target of RHOA. Further mechanistic investigation showed that RHOA activation leads to relocation of the serum response factor (SRF) into the nucleus, where it directly activates IGFBP2. Knockout of IGFBP2 in CML cells suppressed cell adhesion/invasion, as well as leukemogenesis in vivo. This elevated IGFBP2 expression was confirmed in primary CML samples. Thus, we demonstrate one mechanism whereby the RHOA-SRF-IGFBP2 signaling axis contributes to the development of leukemia in cells expressing the p210 BCR-ABL1 fusion kinase

Orbital-Dependent Electron Correlation in Double-Layer Nickelate La3Ni2O7

The latest discovery of high temperature superconductivity near 80K in La3Ni2O7 under high pressure has attracted much attention. Many proposals are put forth to understand the origin of superconductivity. The determination of electronic structures is a prerequisite to establish theories to understand superconductivity in nickelates but is still lacking. Here we report our direct measurement of the electronic structures of La3Ni2O7 by high-resolution angle-resolved photoemmission spectroscopy. The Fermi surface and band structures of La3Ni2O7 are observed and compared with the band structure calculations. A flat band is formed from the Ni-3dz2 orbitals around the zone corner which is 50meV below the Fermi level. Strong electron correlations are revealed which are orbital- and momentum-dependent. Our observations will provide key information to understand the origin of high temperature superconductivity in La3Ni2O7.Comment: 18 pages, 4 figure