Acclimation potential of Noni (Morinda citrifolia L.) plant to temperature stress is mediated through photosynthetic electron transport rate.

Noni (Morindacitrifolia L.), a tropical, medicinal plant of the family Rubiaceae utilized since 2000 y ago by the Polynesians, is currently facing a major challenge in production vis-a-vis climate change. The worldwide average temperatures continue to fluctuate, resulting in extremely cold winters and hot summers that reduce plant productivity. Photosynthetic apparatus is an exceptionally sensitive component to estimate the degree of damage at contrasting temperatures. The present study was aimed to evaluate the temperature stress response of Noni plant using the chlorophyll a fluorescence OJIP transients (OJIP transients). Results showed the declined photosynthetic pigment pool and reduced functional and structural integrity of the photosynthetic apparatus under very low- and high-temperature treatments. Drastically lower yield parameters such as φ(Po) and φ(Eo), efficiency ψ(Eo) and performance indices - PIabs and PItotal, and accumulation of inactive reaction centers were observed. Consecutively, a lower level of calculated electron transport from PSII to PSI was observed. In contrast, the enhanced δRo indicates that PSI is more thermo-tolerant as compared to PSII. Additionally, very low and high temperatures cause an increase in antenna size (ABS/RC) and the decrease in the amplitude of I to P phase of fluorescence transient. Overall, the photosynthetic apparatus of leaf tissue was more sensitive to low and high temperatures than the developing fruit. The findings of the present study demonstrated the potential role of thylakoid components of the photosynthetic apparatus, which might be crucial in regulating the temperature stress response in the Noni plant, and thereby crop improvement.

Design, Synthesis and Anticancer Activity of Site Specific Short Chain Cationic Peptide.

BACKGROUND: In spite of current progress in treatment methods, cancer is a major source of morbidity and death rate all over the world. Traditional chemotherapeutic agents aim to divide cancerous cells, are often associated with deleterious side effects to healthy cells and tissues. Host defense peptides Cecropin A and B obtained from insects are capable to lyses various types of human cancer cells at peptide concentrations which are not fatal to normal eukaryotic cells. METHODS: In the present work we have designed short chain α-helical linear and cyclic peptide from cecropin A having same cationic charge, hydrophobicity and helicity. Synthesis of designed novel short chain linear (10) and cyclic compound (12) was accomplished by using solution phase method. All the coupling reactions were carried out by using dicyclohexylcarbodiimide (DCC) as the coupling reagent at room temperature in the presence of N-methylmorpholine (NMM) as the base. The Structure of newly synthesized peptidse were elucidated by 1H-NMR, 13C-NMR, FT-IR, FABMS and elemental analysis data.Cytotoxicity of synthesized compound was tested against Dalton's Lymphoma Ascites (DLA), Ehrlich's Ascites Carcinoma (EAC) and MCF-7 cell lines by using MTT assay and 5-FU as reference compound. RESULT: From biological assessment,it was found that short chain cyclicpeptide12 showed high level of cytotoxic activity against DLA and EAC cell lines. CONCLUSION: By utilizing a structure-based rational approach to anticancer peptide design from cecropin A, we were able to develop short chain linear and cyclic peptides having same charge, hydrophobicity and with improved activity. Systematically removing amino acids, we were able to retaining peptide charge and hydrophobicity/hydrophilicity in linear and cyclic peptide which results to optimize the anticancer activity against DLA and EAC cell lines.

A large-scale analysis of alternative splicing reveals a key role of QKI in lung cancer.

Increasing interest has been devoted in recent years to the understanding of alternative splicing in cancer. In this study, we performed a genome-wide analysis to identify cancer-associated splice variants in non-small cell lung cancer. We discovered and validated novel differences in the splicing of genes known to be relevant to lung cancer biology, such as NFIB, ENAH or SPAG9. Gene enrichment analyses revealed an important contribution of alternative splicing to cancer-related molecular functions, especially those involved in cytoskeletal dynamics. Interestingly, a substantial fraction of the altered genes found in our analysis were targets of the protein quaking (QKI), pointing to this factor as one of the most relevant regulators of alternative splicing in non-small cell lung cancer. We also found that ESYT2, one of the QKI targets, is involved in cytoskeletal organization. ESYT2-short variant inhibition in lung cancer cells resulted in a cortical distribution of actin whereas inhibition of the long variant caused an increase of endocytosis, suggesting that the cancer-associated splicing pattern of ESYT2 has a profound impact in the biology of cancer cells. Finally, we show that low nuclear QKI expression in non-small cell lung cancer is an independent prognostic factor for disease-free survival (HR = 2.47; 95% CI = 1.11-5.46, P = 0.026). In conclusion, we identified several splicing variants with functional relevance in lung cancer largely regulated by the splicing factor QKI, a tumor suppressor associated with prognosis in lung cancer.

Identification of alternative splicing events regulated by the oncogenic factor SRSF1 in lung cancer.

Abnormal alternative splicing has been associated with cancer. Genome-wide microarrays can be used to detect differential splicing events. In this study, we have developed ExonPointer, an algorithm that uses data from exon and junction probes to identify annotated cassette exons. We used the algorithm to profile differential splicing events in lung adenocarcinoma A549 cells after downregulation of the oncogenic serine/arginine-rich splicing factor 1 (SRSF1). Data were generated using two different microarray platforms. The PCR-based validation rate of the top 20 ranked genes was 60% and 100%. Functional enrichment analyses found a substantial number of splicing events in genes related to RNA metabolism. These analyses also identified genes associated with cancer and developmental and hereditary disorders, as well as biologic processes such as cell division, apoptosis, and proliferation. Most of the top 20 ranked genes were validated in other adenocarcinoma and squamous cell lung cancer cells, with validation rates of 80% to 95% and 70% to 75%, respectively. Moreover, the analysis allowed us to identify four genes, ATP11C, IQCB1, TUBD1, and proline-rich coiled-coil 2C (PRRC2C), with a significantly different pattern of alternative splicing in primary non-small cell lung tumors compared with normal lung tissue. In the case of PRRC2C, SRSF1 downregulation led to the skipping of an exon overexpressed in primary lung tumors. Specific siRNA downregulation of the exon-containing variant significantly reduced cell growth. In conclusion, using a novel analytical tool, we have identified new splicing events regulated by the oncogenic splicing factor SRSF1 in lung cancer.