scholarly journals Overexpression of SHORT-ROOT2 transcription factor enhanced the outgrowth of mature axillary buds in poplar trees

2021 ◽  
Author(s):  
Minglei Yi ◽  
Heyu Yang ◽  
Shaohui Yang ◽  
Jiehua Wang
Keyword(s):  
Hybrid Poplar ◽  
Axillary Buds ◽  
Phenotypic Characterization ◽  
Bud Burst ◽  
Wild Type ◽  
Cytokinin Biosynthesis ◽  
Expression Of Genes ◽  
Poplar Trees ◽  
Lower Ratio ◽  
Bud Initiation

Plant branching is usually prevented by an actively proliferating apex. In poplars, one GRAS family member, SHORT-ROOT2 (PtSHR2), was preferentially expressed in axillary buds (AXBs) and was inducible during bud maturation and activation. Overexpression of PtSHR2 (PtSHR2OE) in hybrid poplar impaired the apical dominance and simultaneously promoted the outgrowth of axillary branches below the maturation point (BMP), accompanied by regulated expression of genes critical for axillary meristem initiation and bud formation. Following a detained phenotypic characterization, we compared the IAA and trans-zeatin levels in apical shoots and AXBs of wild-type and PtSHR2OE trees, together with gene expression analyses and defoliation, decapitation, and hormone reapplication assays. PtSHR2OE AXBs contained a significantly lower ratio of auxin to cytokinin than wild-type AXBs, particularly in those below the BMP. Decapitation induced a faster bud burst in PtSHR2OE trees than in wild-type plants, and it could be strongly inhibited by exogenously applied auxin and cytokinin biosynthesis inhibitor, but only partially inhibited by N-1-naphthylphthalamic acid (NPA). An impaired basipetal auxin transport, rather than an insufficient auxin biosynthesis or auxin insensitivity, disturbed the local hormonal homeostasis in PtSHR2OE AXBs, which in turn enhanced the axillary bud initiation and promoted the bud release.

scholarly journals Alopecia in Harlequin mutant mice is associated with reduced AIF protein levels and expression of retroviral elements

2020 ◽  
Author(s):  
Maik Hintze ◽  
Sebastian Griesing ◽  
Marion Michels ◽  
Birgit Blanck ◽  
Lena Wischhof ◽  
...  
Keyword(s):  
Hair Growth ◽  
Transcriptional Regulators ◽  
Mutant Mice ◽  
Wild Type ◽  
Protein Levels ◽  
Expression Of Genes ◽  
Genes Encoding ◽  
Keratinocyte Cell ◽  
Apoptosis Inducing Factor ◽  
Hair Cortex

AbstractWe investigated the contribution of apoptosis-inducing factor (AIF), a key regulator of mitochondrial biogenesis, in supporting hair growth. We report that pelage abnormalities developed during hair follicle (HF) morphogenesis in Harlequin (Hq) mutant mice. Fragility of the hair cortex was associated with decreased expression of genes encoding structural hair proteins, though key transcriptional regulators of HF development were expressed at normal levels. Notably, Aifm1 (R200 del) knockin males and Aifm1(R200 del)/Hq females showed minor hair defects, despite substantially reduced AIF levels. Furthermore, we cloned the integrated ecotropic provirus of the Aifm1Hq allele. We found that its overexpression in wild-type keratinocyte cell lines led to down-regulation of HF-specific Krt84 and Krtap3-3 genes without altering Aifm1 or epidermal Krt5 expression. Together, our findings imply that pelage paucity in Hq mutant mice is mechanistically linked to severe AIF deficiency and is associated with the expression of retroviral elements that might potentially influence the transcriptional regulation of structural hair proteins.

Groundwater Capture Using Hybrid Poplar Trees: Evaluation of a System in Ogden, Utah

2001 ◽  
Vol 3 (1) ◽  
pp. 87-104 ◽  
Author(s):  
A. Ferro ◽  
J. Chard ◽  
R. Kjelgren ◽  
B. Chard ◽  
D. Turner ◽  
...  
Keyword(s):  
Hybrid Poplar ◽  
Poplar Trees

Diverse developmental mutants revealed in an activation-tagged population of poplarThis article is one of a selection of papers published on the Special Issue of Poplar Research in Canada.

2007 ◽  
Vol 85 (11) ◽  
pp. 1071-1081 ◽  
Author(s):  
Edward J. Harrison ◽  
Michael Bush ◽  
Jonathan M. Plett ◽  
Daniel P. McPhee ◽  
Robin Vitez ◽  
...  
Keyword(s):  
Large Scale ◽  
Insertional Mutagenesis ◽  
Hybrid Poplar ◽  
Activation Tagging ◽  
Developmental Abnormalities ◽  
Endogenous Gene ◽  
Developmental Mutants ◽  
Poplar Trees ◽  
Wide Range ◽  
Mutant Lines

We have produced the largest population of activation-tagged poplar trees to date, approximately 1800 independent lines, and report on phenotypes of interest that have been identified in tissue culture and greenhouse conditions. Activation tagging is an insertional mutagenesis technique that results in the dominant upregulation of an endogenous gene. A large-scale Agrobacterium -mediated transformation protocol was used to transform the pSKI074 activation-tagging vector into Populus tremula × Populus alba hybrid poplar. We have screened the first 1000 lines for developmental abnormalities and have a visible mutant frequency of 2.4%, with alterations in leaf and stem structure as well as overall stature. Most of the phenotypes represent new phenotypes that have not previously been identified in poplar and, in some cases, not in any other plant either. Molecular analysis of the T-DNA inserts of a subpopulation of mutant lines reveal both single and double T-DNA inserts with double inserts more common in lines with visible phenotypes. The broad range of developmental mutants identified in this pilot screen of the population reveals that it will be a valuable resource for gene discovery in poplar. The full value of this population will only be realized as we screen these lines for a wide range of phenotypes.

YakA, a protein kinase required for the transition from growth to development in Dictyostelium

Development ◽  
1998 ◽  
Vol 125 (12) ◽  
pp. 2291-2302 ◽  
Author(s):  
G.M. Souza ◽  
S. Lu ◽  
A. Kuspa
Keyword(s):  
Cell Cycle ◽  
Protein Kinase ◽  
Basic Protein ◽  
Mrna Levels ◽  
Wild Type ◽  
E Coli ◽  
Cycle Arrest ◽  
Expression Of Genes ◽  
Extracellular Signal ◽  
Nutrient Rich Medium

When Dictyostelium cells starve they arrest their growth and induce the expression of genes necessary for development. We have identified and characterized a protein kinase, YakA, that is essential for the proper regulation of both events. Amino acid sequence and functional similarities indicate that YakA is a homolog of Yak1p, a growth-regulating protein kinase in S. cerevisiae. Purified YakA expressed in E. coli is able to phosphorylate myelin basic protein. YakA-null cells are smaller and their cell cycle is accelerated relative to wild-type cells. When starved, YakA-null cells fail to decrease the expression of the growth-stage gene cprD, and do not induce the expression of genes required for the earliest stages of development. YakA mRNA levels increase during exponential growth and reach a maximum at the point of starvation, consistent with a role in mediating starvation responses. YakA mRNA also accumulates when cells are grown in medium conditioned by cells grown to high density, suggesting that yakA expression is under the control of an extracellular signal that accumulates during growth. Expression of yakA from a conditional promoter causes cell-cycle arrest in nutrient-rich medium and promotes developmental events, such as the expression of genes required for cAMP signaling. YakA appears to regulate the transition from growth to development in Dictyostelium.

scholarly journals Role of CpALS4790 and CpALS0660 in Candida parapsilosis Virulence: Evidence from a Murine Model of Vaginal Candidiasis

2020 ◽  
Vol 6 (2) ◽  
pp. 86
Author(s):  
Marina Zoppo ◽  
Fabrizio Fiorentini ◽  
Cosmeri Rizzato ◽  
Mariagrazia Di Luca ◽  
Antonella Lupetti ◽  
...  
Keyword(s):  
Cell Wall ◽  
Murine Model ◽  
Type Strain ◽  
Wild Type Strain ◽  
Candida Parapsilosis ◽  
Vaginal Candidiasis ◽  
Phenotypic Characterization ◽  
Wild Type ◽  
Mutant Strains

The Candida parapsilosis genome encodes for five agglutinin-like sequence (Als) cell-wall glycoproteins involved in adhesion to biotic and abiotic surfaces. The work presented here is aimed at analyzing the role of the two still uncharacterized ALS genes in C. parapsilosis, CpALS4790 and CpALS0660, by the generation and characterization of CpALS4790 and CpALS066 single mutant strains. Phenotypic characterization showed that both mutant strains behaved as the parental wild type strain regarding growth rate in liquid/solid media supplemented with cell-wall perturbing agents, and in the ability to produce pseudohyphae. Interestingly, the ability of the CpALS0660 null mutant to adhere to human buccal epithelial cells (HBECs) was not altered when compared with the wild-type strain, whereas deletion of CpALS4790 led to a significant loss of the adhesion capability. RT-qPCR analysis performed on the mutant strains in co-incubation with HBECs did not highlight significant changes in the expression levels of others ALS genes. In vivo experiments in a murine model of vaginal candidiasis indicated a significant reduction in CFUs recovered from BALB/C mice infected with each mutant strain in comparison to those infected with the wild type strain, confirming the involvement of CpAls4790 and CpAls5600 proteins in C. parapsilosis vaginal candidiasis in mice.

scholarly journals Loss of resistin ameliorates hyperlipidemia and hepatic steatosis in leptin-deficient mice

2008 ◽  
Vol 295 (2) ◽  
pp. E331-E338 ◽  
Author(s):  
Neel S. Singhal ◽  
Rajesh T. Patel ◽  
Yong Qi ◽  
Yun-Sik Lee ◽  
Rexford S. Ahima
Keyword(s):  
Hepatic Steatosis ◽  
High Fat Diet ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Wild Type ◽  
The Metabolic Syndrome ◽  
Expression Of Genes ◽  
Similar Body ◽  
Deficient Mice

Resistin has been linked to components of the metabolic syndrome, including obesity, insulin resistance, and hyperlipidemia. We hypothesized that resistin deficiency would reverse hyperlipidemia in genetic obesity. C57Bl/6J mice lacking resistin [resistin knockout (RKO)] had similar body weight and fat as wild-type mice when fed standard rodent chow or a high-fat diet. Nonetheless, hepatic steatosis, serum cholesterol, and very low-density lipoprotein (VLDL) secretion were decreased in diet-induced obese RKO mice. Resistin deficiency exacerbated obesity in ob/ob mice, but hepatic steatosis was drastically attenuated. Moreover, the levels of triglycerides, cholesterol, insulin, and glucose were reduced in ob/ob-RKO mice. The antisteatotic effect of resistin deficiency was related to reductions in the expression of genes involved in hepatic lipogenesis and VLDL export. Together, these results demonstrate a crucial role of resistin in promoting hepatic steatosis and hyperlipidemia in obese mice.

scholarly journals Sexual Differentiation Is Coordinately Regulated by Cryptococcus neoformans CRK1 and GAT1

Genes ◽  
2020 ◽  
Vol 11 (6) ◽  
pp. 669
Author(s):  
Kuang-Hung Liu ◽  
Wei-Chiang Shen
Keyword(s):  
Cryptococcus Neoformans ◽  
Sexual Differentiation ◽  
Regulatory Networks ◽  
Genetic Interaction ◽  
Negative Regulator ◽  
Wild Type ◽  
Basidiomycetous Fungus ◽  
Regulatory Circuit ◽  
Expression Of Genes ◽  
In The Wild

The heterothallic basidiomycetous fungus Cryptococcus neoformans has two mating types, MATa and MATα. Morphological progression of bisexual reproduction in C. neoformans is as follows: yeast to hyphal transition, filament extension, basidium formation, meiosis, and sporulation. C. neoformans Cdk-related kinase 1 (CRK1) is a negative regulator of bisexual mating. In this study, we characterized the morphological features of mating structures in the crk1 mutant and determined the genetic interaction of CRK1 in the regulatory networks of sexual differentiation. In the bilateral crk1 mutant cross, despite shorter length of filaments than in the wild-type cross, dikaryotic filaments and other structures still remained intact during bisexual mating, but the timing of basidium formation was approximately 18 h earlier than in the cross between wild type strains. Furthermore, gene expression analyses revealed that CRK1 modulated the expression of genes involved in the progression of hyphal elongation, basidium formation, karyogamy and meiosis. Phenotypic results showed that, although deletion of C. neoformans CRK1 gene increased the efficiency of bisexual mating, filamentation in the crk1 mutant was blocked by MAT2 or ZNF2 mutation. A bioinformatics survey predicted the C. neoformans GATA transcriptional factor Gat1 as a potential substrate of Crk1 kinase. Our genetic and phenotypic findings revealed that C. neoformans GAT1 and CRK1 formed a regulatory circuit to negatively regulate MAT2 to control filamentation progression and transition during bisexual mating.

scholarly journals Comparative Phenotypic Assessment of Cardiac Pathology, Physiology, and Gene Expression in C3H/HeJ, C57BL/6J, and B6C3F1/J Mice

2010 ◽  
Vol 38 (6) ◽  
pp. 923-942 ◽  
Author(s):  
Scott S. Auerbach ◽  
Reuben Thomas ◽  
Ruchir Shah ◽  
Hong Xu ◽  
Molly K. Vallant ◽  
...  
Keyword(s):  
Gene Expression ◽  
Enrichment Analysis ◽  
Phenotypic Characterization ◽  
Low Grade ◽  
Pathway Network ◽  
Cardiac Phenotype ◽  
Expression Of Genes ◽  
Genomic Studies ◽  
Histopathologic Analysis ◽  
Genetically Determined

Human cardiomyopathies often lead to heart failure, a major cause of morbidity and mortality in industrialized nations. Described here is a phenotypic characterization of cardiac function and genome-wide expression from C3H/HeJ, C57BL/6J, and B6C3F1/J male mice. Histopathologic analysis identified a low-grade background cardiomyopathy (murine progressive cardiomyopathy) in eight of nine male C3H/HeJ mice (age nine to ten weeks), but not in male C57BL/6J and in only of ten male B6C3F1/J mice. The C3H/HeJ mouse had an increased heart rate and a shorter RR interval compared to the B6C3F1/J and C57BL/6J mice. Cardiac genomic studies indicated the B6C3F1/J mice exhibited an intermediate gene expression phenotype relative to the 2 parental strains. Disease-centric enrichment analysis indicated a number of cardiomyopathy-associated genes were induced in B6C3F1/J and C3H/HeJ mice, including Myh7, My14, and Lmna and also indicated differential expression of genes associated with metabolic (e.g., Pdk2) and hypoxic stress (e.g. Hif1a). A novel coexpression and integrated pathway network analysis indicated Prkaa2, Pdk2, Rhoj, and Sgcb are likely to play a central role in the pathophysiology of murine progressive cardiomyopathy in C3H/HeJ mice. Our studies indicate that genetically determined baseline differences in cardiac phenotype have the potential to influence the results of cardiotoxicity studies.

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