62 research outputs found

    Complementation of wild strawberry (Fragaria vesca L.) SPATULA (FvSPT) and SPIRAL (FvSPR) genes in Arabidopsis thaliana

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    This study assessed the function of genes involved in wild strawberry (Fragaria vesca L.) fruit development and maturation to better understand the mechanism of non-climacteric fruit ripening. SPATULA (FvSPT) and SPIRAL (FvSPR) genes of Fragaria vesca displayed differential expression between the green and red ripening stages. SPT, which encodes a bHLH transcription factor, was characterized in Arabidopsis thaliana L. where its recessive mutation caused degenerative carpel and fruit development. The spt mutant of A. thaliana had shorter, smaller, and wider spatula-shaped siliques than the wild type. SPT was expressed throughout the development of marginal and transmission tract tissues, confirming its role in regulating the growth of these tissues. Two A. thaliana SPIRAL genes, SPR1 and SPR2, are required for directional control of cell elongation. Recessive mutations in either of these genes decreased anisotropic growth of endodermal and cortical root cells and etiolated hypocotyls and caused right-handed helical growth in epidermal cells. The strawberry SPATULA (FvSPT) and SPIRAL (FvSPR) genes were amplified and spt and spr mutant A. thaliana plants were transformed with FvSPT::pGWB401, FvSPR1-1::pGWB401 and FvSPR1-2::pGWB401 vector constructs. Silique length and seed number/silique in the A. thaliana spt mutant were effectively complemented by FvSPT whereas spr was almost fully complemented by FvSPR1-2, but not by FvSPR1-1

    Promoter analysis of the SPATULA (FvSPT) and SPIRAL (FvSPR) genes in the woodland diploid strawberry (Fragaria vesca L.)

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    The aim of this study was to identify transcription factor (TF) binding sites and cis-regulatory elements (CREs) on the promoters of FvSPR1-like2 (SPIRAL) and FvSPT (SPATULA) genes in the woodland diploid strawberry (Fragaria vesca L.). We identified: (1) MYB59, WRKY25 and WRKY8 TFs which play a role in ethylene signaling; (2) ARF family of TFs which play a role in ARF-mediated auxin signaling on the promoter of FvSPR1-like2 gene; (3) ARR family of TFs which play a role in cytokinin signaling; (4) ERF family of TFs which play a role in ethylene signaling on the promoter of FvSPT. This bioinformatic analysis of TFs and CREs may provide a better understanding of the function of genes involved in, and the mechanism underlying, non-climateric ripening during strawberry fruit maturation

    Shoot tip necrosis of in vitro plant cultures: a reappraisal of possible causes and solutions

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    Shoot tip necrosis is a physiological condition and disorder that can arise in plantlets or shoots in vitro that results in death of the shoot tip. This condition, which can spread basipetally and affect the emergence of axillary shoots from buds lower down the stem, is due to the cessation of apical dominance. STN can occur at both shoot multiplication and rooting stages. One of the most common factors that cause STN is nutrient deficiency or imbalance. Moreover, the presence or absence of plant growth regulators (auxins or cytokinins) at specific developmental stages may impact STN. The cytokinin to auxin ratio within an in vitro plant can be modified by varying the concentration of cytokinins used in the culture medium. The supply of nutrients to in vitro shoots or plantlets might also affect their hormonal balance, thus modifying the occurrence of STN. High relative humidity within culture vessels and hyperhydricity are associated with STN. An adequate supply of calcium as the divalent cation (Ca2+) can hinder STN by inhibiting the accumulation of phenolic compounds and thus programmed cell death. Moreover, the level of Ca2+ affects auxin transport and ethylene production, and higher ethylene production, which can occur as a result of high relative humidity in or poor ventilation of the in vitro culture vessel, induces STN. High relative humidity can decrease the mobility of Ca2+ within a plant, resulting in Ca2+ deficiency and STN. STN of in vitro shoots or plantlets can be halted or reversed by altering the basal medium, mainly the concentration of Ca2+, adjusting the levels of auxins or cytokinins, or modifying culture conditions. This review examines the literature related to STN, seeks to discover the associated factors and relations between them, proposes practical solutions, and attempts to better understand the mechanism(s) underlying this condition in vitroThis research was financed by the Higher Education Institutional Excellence Programme (NKFIH-1150-6/2019) of the Ministry of Innovation and Technology in Hungary, within the framework of the Biotechnology thematic programme of the University of Debrecen. The study and submission for publication were approved by the University of Debrecen (BPTR/DEENK/0008/2019). Esmaeil Nezami-Alanagh thanks the Biotechnology Department at Imam Khomeini International University (IKIU) for their assistance in carrying out a part of the experiment work and also to Science and Technology Park of East-Azarbaijan, Islamic Republic of Iran, for financial support. The Spanish work on STN modeling was funded by Xunta de Galicia, Spain (CITACA Strategic Partnership, Reference: ED431E 2018/07 and REDES, Reference: ED431D-2017/19)S

    Network Analysis of Oyster Transcriptome Revealed a Cascade of Cellular Responses during Recovery after Heat Shock

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    Oysters, as a major group of marine bivalves, can tolerate a wide range of natural and anthropogenic stressors including heat stress. Recent studies have shown that oysters pretreated with heat shock can result in induced heat tolerance. A systematic study of cellular recovery from heat shock may provide insights into the mechanism of acquired thermal tolerance. In this study, we performed the first network analysis of oyster transcriptome by reanalyzing microarray data from a previous study. Network analysis revealed a cascade of cellular responses during oyster recovery after heat shock and identified responsive gene modules and key genes. Our study demonstrates the power of network analysis in a non-model organism with poor gene annotations, which can lead to new discoveries that go beyond the focus on individual genes
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