Single nucleotide polymorphisms in intron 5 of the feline myosin regulatory light chain gene detected by SSCP analysis

2000 ◽  
Vol 31 (4) ◽  
pp. 281-282
Author(s):  
A L Magnon ◽  
K M Meurs ◽  
M D Kittleson ◽  
W A Ware
Gene ◽  
2001 ◽  
Vol 263 (1-2) ◽  
pp. 141-149 ◽  
Author(s):  
Juliette Ravaux ◽  
Alexandre Hassanin ◽  
Jean Deutsch ◽  
Françoise Gaill ◽  
Ulrich Markmann-Mulisch

Insects ◽  
2020 ◽  
Vol 11 (12) ◽  
pp. 844
Author(s):  
Zhenqi Tian ◽  
Yan Zhang ◽  
Chao Ma ◽  
Hongsong Chen ◽  
Jianying Guo ◽  
...  

Ambrosia artemisiifolia is a noxious invasive alien weed, that is harmful to the environment and human health. Ophraella communa is a biocontrol agent for A. artemisiifolia, that was accidentally introduced to the Chinese mainland and has now spread throughout southern China. Recently, we found that upon artificial introduction, O. communa can survive in northern China as well. Therefore, it is necessary to study the cold hardiness of O. communa. Many genes have been identified to play a role in cold-tolerance regulation in insects, but the function of the gene encoding non-muscle myosin regulatory light chain (MRLC-sqh) remains unknown. To evaluate the role played by MRLC-sqh in the cold-tolerance response, we cloned and characterized MRLC-sqh from O. communa. Quantitative real-time PCR revealed that MRLC-sqh was expressed at high levels in the gut and pupae of O. communa. The expression of MRLC-sqh was shown to decrease after cold shock between 10 and 0 °C and ascend between 0 and −10 °C, but these did not show a positive association between MRLC-sqh expression and cold stress. Silencing of MRLC-sqh using dsMRLC-sqh increased the chill-coma recovery time of these beetles, suggesting that cold hardiness was reduced in its absence. These results suggest that the cold hardiness of O. communa may be partly regulated by MRLC-sqh. Our findings highlight the importance of motor proteins in mediating the cold response in insects.


2001 ◽  
Vol 68 (1) ◽  
pp. 214-218 ◽  
Author(s):  
Tomonari Sasaki ◽  
Tomoko Tahira ◽  
Akari Suzuki ◽  
Koichiro Higasa ◽  
Yoji Kukita ◽  
...  

2017 ◽  
Vol 15 (4) ◽  
pp. 492-495 ◽  
Author(s):  
Roberta Cardoso Petroni ◽  
Susana Elaine Alves da Rosa ◽  
Flavia Pereira de Carvalho ◽  
Rúbia Anita Ferraz Santana ◽  
Joyce Esteves Hyppolito ◽  
...  

ABSTRACT Hereditary hyperferritinemia-cataract syndrome is an autosomal dominant genetic disorder associated with mutations in the 5’UTR region of the ferritin light chain gene. These mutations cause the ferritin levels to increase even in the absence of iron overload. Patients also develop bilateral cataract early due to accumulation of ferritin in the lens, and many are misdiagnosed as having hemochromatosis and thus not properly treated. The first cases were described in 1995 and several mutations have already been identified. However, this syndrome is still a poorly understood. We report two cases of unrelated Brazilian families with clinical suspicion of the syndrome, which were treated in our department. For the definitive diagnosis, the affected patients, their parents and siblings were submitted to Sanger sequencing of the 5’UTR region for detection of the ferritin light gene mutation. Single nucleotide polymorphism-like mutations were found in the affected patients, previously described. The test assisted in making the accurate diagnosis of the disease, and its description is important so that the test can be incorporated into clinical practice.


1999 ◽  
Vol 146 (2) ◽  
pp. 439-451 ◽  
Author(s):  
Christopher A. Shelton ◽  
J. Clayton Carter ◽  
Gregory C. Ellis ◽  
Bruce Bowerman

Using RNA-mediated genetic interference in a phenotypic screen, we identified a conserved nonmuscle myosin II regulatory light chain gene in Caenorhabditis elegans, which we name mlc-4. Maternally supplied mlc-4 function is required for cytokinesis during both meiosis and mitosis and for establishment of anterior-posterior (a-p) asymmetries after fertilization. Reducing the function of mlc-4 or nmy-2, a nonmuscle myosin II gene, also leads to a loss of polarized cytoplasmic flow in the C. elegans zygote, supporting models in which cytoplasmic flow may be required to establish a-p differences. Germline P granule localization at the time of cytoplasmic flow is also lost in these embryos, although P granules do become localized to the posterior pole after the first mitosis. This result suggests that a mechanism other than cytoplasmic flow or mlc-4/nmy-2 activity can generate some a-p asymmetries in the C. elegans zygote. By isolating a deletion allele, we show that removing zygotic mlc-4 function results in an elongation phenotype during embryogenesis. An mlc-4/green fluorescent protein transgene is expressed in lateral rows of hypodermal cells and these cells fail to properly change shape in mlc-4 mutant animals during elongation.


2010 ◽  
Vol 34 (8) ◽  
pp. S75-S75
Author(s):  
Weifeng Zhu ◽  
Zhuoqi Liu ◽  
Daya Luo ◽  
Xinyao Wu ◽  
Fusheng Wan

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