Role of the regulatory genes SEF1, VMA1 and SFU1 in riboflavin synthesis in the flavinogenic yeast Candida famata (Candida flareri)

Yeast ◽  
2020 ◽  
Vol 37 (9-10) ◽  
pp. 497-504
Author(s):  
Yuliia Andreieva ◽  
Yana Petrovska ◽  
Oleksii Lyzak ◽  
Wen Liu ◽  
Yingqian Kang ◽  
...  
2021 ◽  
Author(s):  
Zhiwei Luo ◽  
Bart J Janssen ◽  
Kimberley C Snowden

One sentence summary The key regulatory genes and the role of multiple plant hormones coordinate the process of axillary meristem initiation and subsequent growth into a branch.


2019 ◽  
Vol 10 ◽  
Author(s):  
Kevin Sean O’Connell ◽  
Nathaniel Wade McGregor ◽  
Robin Emsley ◽  
Soraya Seedat ◽  
Louise Warnich

2003 ◽  
Vol 185 (18) ◽  
pp. 5465-5472 ◽  
Author(s):  
Yuki Katayama ◽  
Hong-Zhong Zhang ◽  
Dong Hong ◽  
Henry F. Chambers

ABSTRACT Although the staphylococcal methicillin resistance determinant, mecA, resides on a mobile genetic element, staphylococcus cassette chromosome mec (SCCmec), its distribution in nature is limited to as few as five clusters of related methicillin-resistant Staphylococcus aureus (MRSA) clones. To investigate the potential role of the host chromosome in clonal restriction of the methicillin resistance determinant, we constructed plasmid pYK20, carrying intact mecA, and introduced it into several methicillin-susceptible Staphylococcus aureus strains, five of which were naive hosts (i.e., mecA not previously resident on the host chromosome) and five of which were experienced hosts (i.e., methicillin-susceptible variants of MRSA strains from which SCCmec was excised). We next assessed the effect of the recipient background on the methicillin resistance phenotype by population analysis, by assaying the mecA expression of PBP2a by Western blot analysis, and by screening for mutations affecting mecA. Each experienced host transformed with pYK20 had a resistance phenotype and expressed PBP2a similar to that of the parent with chromosomal SCCmec, but naive hosts transformed with pYK20 selected against its expression, indicative of a host barrier. Either inducible β-lactamase regulatory genes blaR1-blaI or homologous regulatory genes mecR1-mecI, which control mecA expression, acted as compensatory elements, permitting the maintenance and expression of plasmid-carried mecA.


Blood ◽  
2007 ◽  
Vol 109 (11) ◽  
pp. 5027-5035 ◽  
Author(s):  
Sara Gardenghi ◽  
Maria F. Marongiu ◽  
Pedro Ramos ◽  
Ella Guy ◽  
Laura Breda ◽  
...  

Abstract Progressive iron overload is the most salient and ultimately fatal complication of β-thalassemia. However, little is known about the relationship among ineffective erythropoiesis (IE), the role of iron-regulatory genes, and tissue iron distribution in β-thalassemia. We analyzed tissue iron content and iron-regulatory gene expression in the liver, duodenum, spleen, bone marrow, kidney, and heart of mice up to 1 year old that exhibit levels of iron overload and anemia consistent with both β-thalassemia intermedia (th3/+) and major (th3/th3). Here we show, for the first time, that tissue and cellular iron distribution are abnormal and different in th3/+ and th3/th3 mice, and that transfusion therapy can rescue mice affected by β-thalassemia major and modify both the absorption and distribution of iron. Our study reveals that the degree of IE dictates tissue iron distribution and that IE and iron content regulate hepcidin (Hamp1) and other iron-regulatory genes such as Hfe and Cebpa. In young th3/+ and th3/th3 mice, low Hamp1 levels are responsible for increased iron absorption. However, in 1-year-old th3/+ animals, Hamp1 levels rise and it is rather the increase of ferroportin (Fpn1) that sustains iron accumulation, thus revealing a fundamental role of this iron transporter in the iron overload of β-thalassemia.


Yeast ◽  
2004 ◽  
Vol 21 (15) ◽  
pp. 1307-1316 ◽  
Author(s):  
Andriy Y. Voronovsky ◽  
Charles A. Abbas ◽  
Kostyantyn V. Dmytruk ◽  
Olena P. Ishchuk ◽  
Barbara V. Kshanovska ◽  
...  

Genetica ◽  
1984 ◽  
Vol 52-53 (1) ◽  
pp. 1-15 ◽  
Author(s):  
F. J. Ayala ◽  
J. F. McDonald

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 3509-3509
Author(s):  
Silja D. Andradottir ◽  
Magnus K. Magnusson

Abstract Constitutively activated fusion tyrosine kinases of the Platelet-dervied growth factor β receptor (PDGFβR) family have been described in patients with chronic myelomonocytic leukemia (CMML). Like other tyrosine kinase driven myeloproliferative syndromes, CMML is characterized by progression leading to highly aggressive acute leukemia. In order to understand the progression of these malignancies we are studying tyrosine kinase pathway regulatory genes. In this study we focus on the functional role of the sprouty gene family in the regulation of PDGFβR fusion oncogenes. Sprouty (Spry) has recently been identified as a repressor of receptor tyrosine kinases signaling in vertebrates and invertebrates. The studies of sprouty in the mammalian system have thus far mostly focused on the regulation of the epidermal and fibroblast growth factor receptor, while nothing is known about the possible regulation of PDGF receptors by sprouty proteins and nothing is known about regulation of mutationally activated tyrosine kinases. Expression plasmids containing human sprouty wildtype genes (Spry1-3 WT) were constructed, along with a series of plasmids containing dominant negative variants by site-direct mutagenesis in critically conserved domains [Spry1(Y53F), Spry2(Y55F), Spry3(Y27F)]. Stable cell lines containing these plasmids have been generated in the BaF3 background with or without the constitutively activated Rabaptin-5/PDGFβR (R/P) fusion oncoprotein. Effects on cell growth and downstream signaling events were studied. Spry1 WT and Spry3 WT signifcantly inhibit growth of R/P transformed BaF3 cell lines. This inhibition was much more pronounced in IL3 depleted media indicating that the inhibition is mediated through PDGFβR tyrosine kinase inhibition. The dominant negative forms, Spry1(Y53F) and Spry3(Y27F) stimulated growth of the the same BaF3 cell lines. Results from [3H]thymidine uptake studies in these cell lines showed decreased uptake in Spry1 WT and Spry3 WT transduced cells and increased uptake in the dominant negative forms, indicating that the effects are through increased proliferation rather than decreased apoptosis. Interestingly, R/P transformed BaF3 cell lines transfected with plasmid containing Spry2 WT and Spry2(Y55F) showed inverse results, Spry2 WT stimulated growth while Spry2(Y55F) inhibited growth. A possible explanation for stimulatory effects of Spry2 is that this Spry variant contains a Cbl binding domain previously shown to prevent Cbl mediated ubiquitylation and degradation of RTKs. We are currently studying the downstream targets of the Spry regulation of PDGFβR focusing on Ras and MAPkinase pathways. In conclusion, we have shown that Spry1 and Spry3 inhibits growth of PDGFβR transformed BaF3 cell lines, while Spry2 stimulates growth. This is the first evidence for regulatory role of Sprouty genes in activated fusion tyrosine kinase. This conserved family of tyrosine kinase regulatory genes is an ideal target for studies of disease progression in tyrosine kinase driven malignancies.


2009 ◽  
Vol 18 (8) ◽  
pp. 1211-1220 ◽  
Author(s):  
Sabino Ciavarella ◽  
Franco Dammacco ◽  
Monica De Matteo ◽  
Giuseppe Loverro ◽  
Franco Silvestris

2016 ◽  
Vol 2016 ◽  
pp. 1-14 ◽  
Author(s):  
Katarzyna Licznerska ◽  
Aleksandra Dydecka ◽  
Sylwia Bloch ◽  
Gracja Topka ◽  
Bożena Nejman-Faleńczyk ◽  
...  

Previous studies indicated that these genetic elements could be involved in the regulation of lysogenization and prophage induction processes. The effects were dramatic in Shiga toxin-converting phageΦ24Bafter treatment with oxidative stress-inducing agent, hydrogen peroxide, while they were less pronounced in bacteriophageλand in both phages irradiated with UV. The hydrogen peroxide-caused prophage induction was found to be RecA-dependent. Importantly, in hydrogen peroxide-treatedE. colicells lysogenic for eitherλorΦ24B, deletion of theexo-xisregion resulted in a significant decrease in the levels of expression of the S.O.S. regulon genes. Moreover, under these conditions, a dramatic decrease in the levels of expression of phage genes crucial for lytic development (particularlyxis, exo, N, cro, O, Q, andR) could be observed inΦ24B-, but not inλ-bearing cells. We conclude that genes located in theexo-xisregion are necessary for efficient expression of both host S.O.S regulon in lysogenic bacteria and regulatory genes of Shiga toxin-converting bacteriophageΦ24B.


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