scholarly journals The ERA-related GTPase AtERG2 associated with mitochondria 18S RNA is essential for early embryo development inArabidopsis

2017 ◽  
Author(s):  
Pengyu Cheng ◽  
Hongjuan Li ◽  
Linlin Yuan ◽  
Huiyong Li ◽  
Lele Xi ◽  
...  

AbstractThe ERA (E. coliRAS-like protein)-related GTPase (ERG) is a nuclear-encoded GTPase with two conserved domains: a GTPase domain and a K Homology domain. ERG plays a vital role in early seed development inAntirrhinum majus. However, the mechanism that regulates seed development remains unclear. Blasting the genome sequence revealed two homologies of ERG, AtERG1, and AtERG2 inArabidopsis. In this study, we found that AtERG2 is localised in the mitochondria and binds mitochondrial 18S RNA. Promoter and transcript analyses indicated thatAtERG2was mainly expressed in the leaf vein, trichome, mature pollen, and ovule. The mutants ofAtERG2showed recessive lethal, gametophytic maternal effects, silique shortage, and early seed abortion, in which some seeds arrested in the zygotic stage at 1.5 days after pollination (DAP) and aborted at 2.0 DAP inaterg2-1+/-. Reactive oxygen species (ROS) accumulated at 1.5 DAP in the arrested seeds, and the transcription of several ROS-responsible genes,WRKY40,ANAC017, andAOXla, was up-regulated in theaterg2-1+/- seeds which were arrested 1.5 and 2.0 DAP but not in wild-type (WT) andaterg2-1+/- seeds. The cell death-related gene BAG6 was also transcriptionally activated inaterg2-1+/- seeds arrested at 2.0 DAP. Chloramphenicol treatment during pollination induced a similar phenotype and gene expression pattern but showed no transcriptional changes of ANAC017 in WT. These results suggested thatAtERG2promotes early seed development by affecting the maturation of the mitochondria ribosome small subunit and mitochondrial protein translation inArabidopsis.

1985 ◽  
Vol 27 (2) ◽  
pp. 134-142 ◽  
Author(s):  
J. P. Gustafson ◽  
A. J. Lukaszewski

The early embryo and endosperm development patterns of five annual taxa and three perennial taxa of the genus Secale were analyzed. The results showed that there was considerable variation in the speed of early embryo and endosperm development within the genus Secale, and that the developmental patterns of the annual and perennial taxa overlapped. Comparisons indicated that DNA content per se did not have any influence on the speed of early embryo development or aberrant endosperm nucleus production in either the annual or perennial taxa. However, comparisons between the percent telomeric heterochromatin and the number of embryo cells produced showed a significant positive correlation in the annual taxa, and a nonsignificant correlation in the perennial taxa. There was a positive correlation between the number of aberrant endosperm nuclei and percent telomeric heterochromatin in the annual taxa, while the perennial taxa showed a nonsignificant but negative correlation. The results suggest that percent telomeric heterochromatin has a different effect on early seed development in the annual taxa than in the perennial taxa.Key words: Secale, heterochromatin, DNA content, embryo cell cycle.


1985 ◽  
Vol 27 (5) ◽  
pp. 542-548 ◽  
Author(s):  
J. P. Gustafson ◽  
A. J. Lukaszewski

Considerable variation was observed in the early embryo and endosperm developmental patterns of several Triticum durum × Secale species (africanum, cereale, dighoricum, kuprijanovii, montanum, segetale, vavilovii) amphiploids. However, the Triticum – S. africanum hybrid was the only one which developed at a faster rate than either of its parents. Its endosperm became cellular and began depositing starch at least 24 h before any previously analyzed cereal. The influence of Secale DNA and heterochromatin on the developmental patterns of the amphiploids was exactly the opposite of that in the genus Secale itself (i.e., as the amount of telomeric heterochromatin increases developmental speed decreases). The results, in general, suggest that the control of Secale developmental characteristics, whether they are genotypic or nucleotypic, are suppressed when placed in a wheat background.Key words: triticale, heterochromatin, interspecific hybrid, wheat embryo.


2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Juan Zhao ◽  
Hui Li ◽  
Guangxin Chen ◽  
Lijun Du ◽  
Peiyan Xu ◽  
...  

Abstract Background Aneuploidy is the most frequent cause of early-embryo abortion. Any defect in chromosome segregation would fail to satisfy the spindle assembly checkpoint (SAC) during mitosis, halting metaphase and causing aneuploidy. The mitotic checkpoint complex (MCC), comprising MAD1, MAD2, Cdc20, BUBR1 and BUB3, plays a vital role in SAC activation. Studies have confirmed that overexpression of MAD2 and BUBR1 can facilitate correct chromosome segregation and embryo stability. Research also proves that miR-125b negatively regulates MAD1 expression by binding to its 3′UTR. However, miR-125b, Mad1 and Bub3 gene expression in aneuploid embryos of spontaneous abortion has not been reported to date. Methods In this study, embryonic villi from miscarried pregnancies were collected and divided into two groups (aneuploidy and euploidy) based on High-throughput ligation-dependent probe amplification (HLPA) and Fluorescence in situ hybridization (FISH) analyses. RNA levels of miR-125b, MAD1 and BUB3 were detected by Quantitative real-time PCR (qRT-PCR); protein levels of MAD1 and BUB3 were analysed by Western blotting. Results statistical analysis (p < 0.05) showed that miR-125b and BUB3 were significantly down-regulated in the aneuploidy group compared to the control group and that MAD1 was significantly up-regulated. Additionally, the MAD1 protein level was significantly higher in aneuploidy abortion villus, but BUB3 protein was only mildly increased. Correlation analysis revealed that expression of MAD1 correlated negatively with miR-125b. Conclusion These results suggest that aneuploid abortion correlates positively with MAD1 overexpression, which might be caused by insufficient levels of miR-125b. Taken together, our findings first confirmed the negative regulatory mode between MAD1 and miR-125b, providing a basis for further mechanism researches in aneuploid abortion.


2015 ◽  
Vol 90 (3) ◽  
pp. 249-265 ◽  
Author(s):  
Jiehua Qiu ◽  
Yuxuan Hou ◽  
Xiaohong Tong ◽  
Yifeng Wang ◽  
Haiyan Lin ◽  
...  

Planta ◽  
2007 ◽  
Vol 226 (4) ◽  
pp. 805-813 ◽  
Author(s):  
Roberto Schmidt ◽  
Harald Stransky ◽  
Wolfgang Koch

2007 ◽  
Vol 10 (7) ◽  
pp. 828-837 ◽  
Author(s):  
Takahiro Chihara ◽  
David Luginbuhl ◽  
Liqun Luo

2021 ◽  
Author(s):  
Yuka Murofushi ◽  
Itaru Hayakawa ◽  
Yuichi Abe ◽  
Tatsuyuki Ohto ◽  
Kei Murayama ◽  
...  

Abstract KARS encodes lysyl-tRNA synthetase, which is essential for protein translation. KARS mutations sometimes cause impairment of cytoplasmic and mitochondrial protein synthesis, and sometimes lead to progressive leukodystrophies with mitochondrial signature and psychomotor regression, and follow a rapid regressive course to premature death. There has been no disease-modifying therapy beyond supportive treatment. We present a 5-year-old male patient with an asymmetrical leukodystrophy who showed overt evidence of mitochondrial dysfunction, including elevation of lactate on brain MR spectroscopy and low oxygen consumption rate in fibroblasts. We diagnosed this patient's condition as KARS-related leukodystrophy with cerebral calcification, congenital deafness, and evidence of mitochondrial dysfunction. We employed a ketogenic diet as well as multiple vitamin supplementation with the intention to alleviate mitochondrial dysfunction. The patient showed alleviation of his psychomotor regression and even partial restoration of his abilities within 4 months. This is an early report of a potential disease-modifying therapy for KARS-related progressive leukodystrophy without appreciable adverse effects.


2017 ◽  
Vol 175 (2) ◽  
pp. 758-773 ◽  
Author(s):  
Yanbing Wang ◽  
Tatsuya Tsukamoto ◽  
Jennifer A. Noble ◽  
Xunliang Liu ◽  
Rebecca A. Mosher ◽  
...  

2018 ◽  
Vol 216 (2) ◽  
pp. 253-266 ◽  
Author(s):  
Yuxiang Zheng ◽  
Lewis C. Cantley

Folate metabolism is crucial for many biochemical processes, including purine and thymidine monophosphate (dTMP) biosynthesis, mitochondrial protein translation, and methionine regeneration. These biochemical processes in turn support critical cellular functions such as cell proliferation, mitochondrial respiration, and epigenetic regulation. Not surprisingly, abnormal folate metabolism has been causally linked with a myriad of diseases. In this review, we provide a historical perspective, delve into folate chemistry that is often overlooked, and point out various missing links and underdeveloped areas in folate metabolism for future exploration.


Author(s):  
Fei Wang ◽  
Deyu Zhang ◽  
Dejiu Zhang ◽  
Peifeng Li ◽  
Yanyan Gao

Mitochondria are one of the most important organelles in cells. Mitochondria are semi-autonomous organelles with their own genetic system, and can independently replicate, transcribe, and translate mitochondrial DNA. Translation initiation, elongation, termination, and recycling of the ribosome are four stages in the process of mitochondrial protein translation. In this process, mitochondrial protein translation factors and translation activators, mitochondrial RNA, and other regulatory factors regulate mitochondrial protein translation. Mitochondrial protein translation abnormalities are associated with a variety of diseases, including cancer, cardiovascular diseases, and nervous system diseases. Mutation or deletion of various mitochondrial protein translation factors and translation activators leads to abnormal mitochondrial protein translation. Mitochondrial tRNAs and mitochondrial ribosomal proteins are essential players during translation and mutations in genes encoding them represent a large fraction of mitochondrial diseases. Moreover, there is crosstalk between mitochondrial protein translation and cytoplasmic translation, and the imbalance between mitochondrial protein translation and cytoplasmic translation can affect some physiological and pathological processes. This review summarizes the regulation of mitochondrial protein translation factors, mitochondrial ribosomal proteins, mitochondrial tRNAs, and mitochondrial aminoacyl-tRNA synthetases (mt-aaRSs) in the mitochondrial protein translation process and its relationship with diseases. The regulation of mitochondrial protein translation and cytoplasmic translation in multiple diseases is also summarized.


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