scholarly journals A Dominant Mutation in the Pea PHYA Gene Confers Enhanced Responses to Light and Impairs the Light-Dependent Degradation of Phytochrome A

2004 ◽  
Vol 135 (4) ◽  
pp. 2186-2195 ◽  
Author(s):  
James L. Weller ◽  
Shona L. Batge ◽  
Jennifer J. Smith ◽  
L. Huub J. Kerckhoffs ◽  
Vitaly A. Sineshchekov ◽  
...  
1997 ◽  
Vol 9 (10) ◽  
pp. 1727-1743 ◽  
Author(s):  
S L Anderson ◽  
D E Somers ◽  
A J Millar ◽  
K Hanson ◽  
J Chory ◽  
...  

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Xiang Zhang ◽  
Jiejing Qian ◽  
Huafeng Wang ◽  
Yungui Wang ◽  
Yi Zhang ◽  
...  

AbstractVenetoclax (VEN) plus azacitidine has become the first-line therapy for elderly patients with acute myeloid leukemia (AML), and has a complete remission (CR) plus CR with incomplete recovery of hemogram rate of ≥70%. However, the 3-year survival rate of these patients is < 40% due to relapse caused by acquired VEN resistance, and this remains the greatest obstacle for the maintenance of long-term remission in VEN-sensitive patients. The underlying mechanism of acquired VEN resistance in AML remains largely unknown. Therefore, in the current study, nine AML patients with acquired VEN resistance were retrospectively analyzed. Our results showed that the known VEN resistance-associated BCL2 mutation was not present in our cohort, indicating that, in contrast to chronic lymphocytic leukemia, this BCL2 mutation is dispensable for acquired VEN resistance in AML. Instead, we found that reconstructed existing mutations, especially dominant mutation conversion (e.g., expanded FLT3-ITD), rather than newly emerged mutations (e.g., TP53 mutation), mainly contributed to VEN resistance in AML. According to our results, the combination of precise mutational monitoring and advanced interventions with targeted therapy or chemotherapy are potential strategies to prevent and even overcome acquired VEN resistance in AML.


2004 ◽  
Vol 17 (11) ◽  
pp. 1242-1249 ◽  
Author(s):  
Phil H. Smith ◽  
John A. Howie ◽  
Anthony J. Worland ◽  
Rebecca Stratford ◽  
Lesley A. Boyd

Two mutants were isolated in wheat that showed enhanced resistance towards Puccinia striiformis f. sp. tritici, the fungal causal agent of yellow rust. The altered phenotype of I3-48 is due to a minimum of two mutation events, each showing a partial, additive effect, with one mutation segregating with a deletion on the long arm of chromosome 4D. In the case of I3-54, the enhanced resistance is due to a single, dominant mutation. In both mutants, the expression of the enhanced resistance is growth-stage specific. With I3-54, the full resistance phenotype is apparent from the third seedling leaf onwards, while with I3-48, a full resistance phenotype is only seen on the tenth and subsequent leaves. In addition to the enhanced resistance towards yellow rust, I3-48 also shows enhanced resistance towards brown rust, and I3-54 shows enhanced resistance to powdery mildew.


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