scholarly journals A Protease Sensitive Region of Plant and Animal Ribonucleases Belonging to the RNase T2 Family.

1998 ◽  
Vol 21 (6) ◽  
pp. 634-637 ◽  
Author(s):  
Masanori IWAMA ◽  
Ayumu KUSANO ◽  
Yuko OGAWA ◽  
Kazuko OHGI ◽  
Masachika IRIE
Keyword(s):  
2021 ◽  
Vol 8 (1) ◽  
Author(s):  
Jianke Du ◽  
Chunfeng Ge ◽  
Tingting Li ◽  
Sanhong Wang ◽  
Zhihong Gao ◽  
...  

AbstractStrawberry (Fragaria spp.) is a member of the Rosoideae subfamily in the family Rosaceae. The self-incompatibility (SI) of some diploid species is a key agronomic trait that acts as a basic pollination barrier; however, the genetic mechanism underlying SI control in strawberry remains unclear. Two candidate S-RNases (Sa- and Sb-RNase) identified in the transcriptome of the styles of the self-incompatible Fragaria viridis 42 were confirmed to be SI determinants at the S locus following genotype identification and intraspecific hybridization using selfing progenies. Whole-genome collinearity and RNase T2 family analysis revealed that only an S locus exists in Fragaria; however, none of the compatible species contained S-RNase. Although the results of interspecific hybridization experiments showed that F. viridis (SI) styles could accept pollen from F. mandshurica (self-compatible), the reciprocal cross was incompatible. Sa and Sb-RNase contain large introns, and their noncoding sequences (promotors and introns) can be transcribed into long noncoding RNAs (lncRNAs). Overall, the genus Fragaria exhibits S-RNase-based gametophytic SI, and S-RNase loss occurs at the S locus of compatible germplasms. In addition, a type of SI-independent unilateral incompatibility exists between compatible and incompatible Fragaria species. Furthermore, the large introns and neighboring lncRNAs in S-RNase in Fragaria could offer clues about S-RNase expression strategies.


Genetics ◽  
2000 ◽  
Vol 156 (1) ◽  
pp. 31-44 ◽  
Author(s):  
Burkhard R Braun ◽  
W Steven Head ◽  
Ming X Wang ◽  
Alexander D Johnson

Abstract TUP1 encodes a transcriptional repressor that negatively controls filamentous growth in Candida albicans. Using subtractive hybridization, we identified six genes, termed repressed by TUP1 (RBT), whose expression is regulated by TUP1. One of the genes (HWP1) has previously been characterized, and a seventh TUP1-repressed gene (WAP1) was recovered due to its high similarity to RBT5. These genes all encode secreted or cell surface proteins, and four out of the seven (HWP1, RBT1, RBT5, and WAP1) encode putatively GPI-modified cell wall proteins. The remaining three, RBT2, RBT4, and RBT7, encode, respectively, an apparent ferric reductase, a plant pathogenesis-related protein (PR-1), and a putative secreted RNase T2. The expression of RBT1, RBT4, RBT5, HWP1, and WAP1 was induced in wild-type cells during the switch from the yeast form to filamentous growth, indicating the importance of TUP1 in regulating this process and implicating the RBTs in hyphal-specific functions. We produced knockout strains in C. albicans for RBT1, RBT2, RBT4, RBT5, and WAP1 and detected no phenotypes on several laboratory media. However, two animal models for C. albicans infection, a rabbit cornea model and a mouse systemic infection model, revealed that rbt1Δ and rbt4Δ strains had significantly reduced virulence. TUP1 appears, therefore, to regulate many genes in C. albicans, a significant fraction of which are induced during filamentous growth, and some of which participate in pathogenesis.


2003 ◽  
Vol 278 (14) ◽  
pp. 11811-11817 ◽  
Author(s):  
J. P. Dehaye ◽  
Akos Nagy ◽  
Anita Premkumar ◽  
R. James Turner
Keyword(s):  

2014 ◽  
Vol 136 (7) ◽  
Author(s):  
Shengli Xu ◽  
Haitao Liu ◽  
Xiaofang Wang ◽  
Xiaomo Jiang

Surrogate models are widely used in simulation-based engineering design and optimization to save the computing cost. The choice of sampling approach has a great impact on the metamodel accuracy. This article presents a robust error-pursuing sequential sampling approach called cross-validation (CV)-Voronoi for global metamodeling. During the sampling process, CV-Voronoi uses Voronoi diagram to partition the design space into a set of Voronoi cells according to existing points. The error behavior of each cell is estimated by leave-one-out (LOO) cross-validation approach. Large prediction error indicates that the constructed metamodel in this Voronoi cell has not been fitted well and, thus, new points should be sampled in this cell. In order to rapidly improve the metamodel accuracy, the proposed approach samples a Voronoi cell with the largest error value, which is marked as a sensitive region. The sampling approach exploits locally by the identification of sensitive region and explores globally with the shift of sensitive region. Comparative results with several sequential sampling approaches have demonstrated that the proposed approach is simple, robust, and achieves the desired metamodel accuracy with fewer samples, that is needed in simulation-based engineering design problems.


1985 ◽  
Vol 5 (1) ◽  
pp. 52-58
Author(s):  
R D Gerard ◽  
B A Montelone ◽  
C F Walter ◽  
J W Innis ◽  
W A Scott

A nuclease-sensitive region forms in chromatin containing a 273-base-pair (bp) segment of simian virus 40 DNA encompassing the viral origin of replication and early and late promoters. We have saturated this region with short deletion mutations and compared the nuclease sensitivity of each mutated segment to that of an unaltered segment elsewhere in the partially duplicated mutant. Although no single DNA segment is required for the formation of a nuclease-sensitive region, a deletion mutation (dl45) which disrupted both exact copies of the 21-bp repeats substantially reduced nuclease sensitivity. Deletion mutations limited to only one copy of the 21-bp repeats had little, if any, effect. A mutant (dl135) lacking all copies of the 21- and 72-bp repeats, while retaining the origin of replication and the TATA box, did not exhibit a nuclease-sensitive region. Mutants which showed reduced nuclease sensitivity had this effect throughout the nuclease-sensitive region, not just at the site of the deletion, indicating that although multiple determinants must be responsible for the nuclease-sensitive chromatin structure they do not function with complete independence. Mutant dl9, which lacks the late portion of the 72-bp segment, showed reduced accessibility to BglI, even though the BglI site is 146 bp away from the site of the deletion.


2014 ◽  
Vol 106 (2) ◽  
pp. 467a
Author(s):  
Sandra E. Pineda-Sanabria ◽  
Ian M. Robertson ◽  
Peter C. Holmes ◽  
Brian D. Sykes

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