scholarly journals A Retrotransposon Insertion in GhMML3_D12 Is Likely Responsible for the Lintless Locus li3 of Tetraploid Cotton

2020 ◽  
Vol 11 ◽  
Author(s):  
Wei Chen ◽  
Yan Li ◽  
Shouhong Zhu ◽  
Shengtao Fang ◽  
Lanjie Zhao ◽  
...  

Cotton (Gossypium) seed fibers can be divided into lint (long) or fuzz (very short). Using fiberless (fuzzless-lintless) mutants, the lint initiation gene Li3 was identified by map-based cloning. The gene is an R2R3-MYB transcription factor located on chromosome D12 (GhMML3_D12). Sequence analysis revealed that li3 is a loss-of-function allele containing a retrotransposon insertion in the second exon that completely blocks the gene’s expression. The genetic loci n2 and n3 underlying the recessive fuzzless phenotype in Gossypium hirsutum were also mapped. The genomic location of n3 overlapped with that of the dominant fuzzless locus N1, and n3 appeared to be a loss-of-function allele caused by a single nucleotide polymorphism (SNP) mutation in the coding region of GhMML3_A12. The n2 allele was found to be co-located with li3 and originated from G. babardense. n2 and li3 are possibly the multiple alleles of the GhMML3_D12 gene. Genetic analysis showed that Li3 and N3 are a pair of homologs with additive effects for the initiation of fibers (fuzz or lint). In addition, the presence of another locus was speculated, and it appeared to show an inhibitory effect on the expression of GhMML3. These findings provide new information about the genetic factors affecting the initiation of fibers in cotton.

2020 ◽  
Vol 10 ◽  
Author(s):  
Fan Yan ◽  
Stephen M. Githiri ◽  
Yajing Liu ◽  
Yu Sang ◽  
Qingyu Wang ◽  
...  

2011 ◽  
Vol 11 (1) ◽  
pp. 155 ◽  
Author(s):  
Jason D Gillman ◽  
Ashley Tetlow ◽  
Jeong-Deong Lee ◽  
J Shannon ◽  
Kristin Bilyeu

2019 ◽  
Author(s):  
Fan Yan ◽  
Stephen M. Githiri ◽  
Yu Sang ◽  
Qingyu Wang ◽  
Ryoji Takahashi

Abstract Background Pubescence color of soybean is controlled by two genes, T and Td. In the presence of a dominant T allele, dominant and recessive alleles of the Td locus generate tawny and light tawny (or near-gray) pubescence, respectively. Flavones, responsible for pubescence color, are catalyzed by two copies of flavone synthase II genes (FNS II-1 and FNS II-2). This study was conducted to map and clone the Td gene. Results Genetic and linkage analysis using an F2 population and F3 families derived from a cross between a Clark near-isogenic line with light tawny pubescence (genotype: TT tdtd) and a Harosoy near-isogenic line with tawny pubescence (TT TdTd) revealed a single gene for pubescence color around the end of chromosome 3. Genome sequence alignment of plant introductions revealed an association between premature stop codons in Glyma.03G258700 (R2R3 MYB transcription factor) and recessive td allele. Cultivars and lines having near-gray or light tawny pubescence and a gray pubescence cultivar with td allele had premature stop codons in the gene. These results suggest that Glyma.03G258700 corresponds to the Td gene. It was predominantly expressed in pubescence. Compared to a tawny pubescence line, a near-isogenic line with td allele produced extremely small amounts of transcripts of Glyma.03G258700, FNS II-1, and FNS II-2 in pubescence. The promoter of FNS II-1 and FNS II-2 shared cis-acting regulatory elements for binding of MYB proteins. These results suggest that the wild-type of Glyma.03G258700 protein binds to the promoter of FNS II genes and upregulates their expression, resulting in increased flavone content and deeper pubescence color. In contrast, mutated Glyma.03G258700 protein fails to upregulate the expression of FNS II genes, resulting in decreased flavone content and dilute pubescence color. Conclusions This study revealed that soybean Glyma.03G258700 encoding the R2R3 MYB transcription factor corresponds to the Td gene. The wild type of MYB protein binds to the promoter of FNS II genes and upregulates their expression, resulting in higher flavone content and deeper pubescence color. Loss-of-function mutation of the gene fails to promote expression of FNS II genes, resulting in lower flavone content and dilute pubescence color.


Author(s):  
Junping Yu ◽  
Guolong Zhao ◽  
Wei Li ◽  
Ying Zhang ◽  
Peng Wang ◽  
...  

Abstract Key message Identification and functional analysis of the male sterile gene MS6 in Glycine max. Abstract Soybean (Glycine max (L.) Merr.) is an important crop providing vegetable oil and protein. The male sterility-based hybrid breeding is a promising method for improving soybean yield to meet the globally growing demand. In this research, we identified a soybean genic male sterile locus, MS6, by combining the bulked segregant analysis sequencing method and the map-based cloning technology. MS6, highly expressed in anther, encodes an R2R3 MYB transcription factor (GmTDF1-1) that is homologous to Tapetal Development and Function 1, a key factor for anther development in Arabidopsis and rice. In male sterile ms6 (Ames1), the mutant allele contains a missense mutation, leading to the 76th leucine substituted by histidine in the DNA binding domain of GmTDF1-1. The expression of soybean MS6 under the control of the AtTDF1 promoter could rescue the male sterility of attdf1 but ms6 could not. Additionally, ms6 overexpression in wild-type Arabidopsis did not affect anther development. These results evidence that GmTDF1-1 is a functional TDF1 homolog and L76H disrupts its function. Notably, GmTDF1-1 shows 92% sequence identity with another soybean protein termed as GmTDF1-2, whose active expression also restored the fertility of attdf1. However, GmTDF1-2 is constitutively expressed at a very low level in soybean, and therefore, not able to compensate for the MS6 deficiency. Analysis of the TDF1-involved anther development regulatory pathway showed that expressions of the genes downstream of TDF1 are significantly suppressed in ms6, unveiling that GmTDF1-1 is a core transcription factor regulating soybean anther development.


2004 ◽  
Vol 279 (46) ◽  
pp. 48205-48213 ◽  
Author(s):  
J. Marcela Hernandez ◽  
George F. Heine ◽  
Niloufer G. Irani ◽  
Antje Feller ◽  
Min-Gab Kim ◽  
...  

Author(s):  
Caroline F. Wright ◽  
Nicholas M. Quaife ◽  
Laura Ramos-Hernández ◽  
Petr Danecek ◽  
Matteo P. Ferla ◽  
...  

Blood ◽  
2013 ◽  
Vol 122 (24) ◽  
pp. 3884-3891 ◽  
Author(s):  
German Ott ◽  
Andreas Rosenwald ◽  
Elias Campo

Abstract MYC is a potent oncogene initially identified as the target of the t(8;14)(q24;q32) chromosome translocation in Burkitt lymphoma. MYC gene alterations have been identified in other mature B-cell neoplasms that are usually associated with an aggressive clinical behavior. Most of these tumors originate in cells that do not normally express MYC protein. The oncogenic events leading to MYC up-regulation seem to overcome the inhibitory effect of physiological repressors such as BCL6 or BLIMP1. Aggressive lymphomas frequently carry additional oncogenic alterations that cooperate with MYC dysregulation, likely counteracting its proapoptotic function. The development of FISH probes and new reliable antibodies have facilitated the study of MYC gene alterations and protein expression in large series of patients, providing new clinical and biological perspectives regarding MYC dysregulation in aggressive lymphomas. MYC gene alterations in large B-cell lymphomas are frequently associated with BCL2 or BCL6 translocations conferring a very aggressive behavior. Conversely, MYC protein up-regulation may occur in tumors without apparent gene alterations, and its association with BCL2 overexpression also confers a poor prognosis. In this review, we integrate all of this new information and discuss perspectives, challenges, and open questions for the diagnosis and management of patients with MYC-driven aggressive B-cell lymphomas.


2022 ◽  
Vol 293 ◽  
pp. 110674
Author(s):  
Yiguang Wang ◽  
Li-Jie Zhou ◽  
Yuxi Wang ◽  
Zhiqiang Geng ◽  
Baoqing Ding ◽  
...  

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