We have examined effects of mutations created by transposition of the Mu1 element of maize into genes coding for Adh 1 and Sh 1, by means of allozyme measurements, DNA and RNA hybridization, cloning, and sequencing. From our analysis of mutant alleles we conclude that the element acts both to reduce steady-state levels of RNA and to induce aberrant processing of primary transcripts. We also conclude that genetic background can exert considerable influence in determining the degree to which Mu1 affects these aspects of gene expression.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1002/dvg.1020100606 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Molecular mechanisms underlying allosteric behavior of Escherichia coli DgoR, a GntR/FadR family transcriptional regulator.
Nucleic Acids Res
January 2025
Department of Biological Sciences, Indian Institute of Science Education and Research (IISER) Mohali, Sector 81, Knowledge City, SAS Nagar, Mohali 140306, Punjab, India.
GntR/FadR family featuring an N-terminal winged helix-turn-helix DNA-binding domain and a C-terminal α-helical effector-binding and oligomerization domain constitutes one of the largest families of transcriptional regulators. Several GntR/FadR regulators govern the metabolism of sugar acids, carbon sources implicated in bacterial-host interactions. Although effectors are known for a few sugar acid regulators, the unavailability of relevant structures has left their allosteric mechanism unexplored.
View Article and Find Full Text PDFLoss of does not affect bone and lean tissue in zebrafish.
JBMR Plus
February 2025
Department of Orthopaedic Surgery and Sports Medicine, University of Washington School of Medicine, Seattle, WA 98195, United States.
Human genetic studies have nominated cadherin-like and PC-esterase domain-containing 1 () as a candidate target gene mediating bone mineral density (BMD) and fracture risk heritability. Recent efforts to define the role of in bone in mouse and human models have revealed complex alternative splicing and inconsistent results arising from gene targeting, making its function in bone difficult to interpret. To better understand the role of in adult bone mass and morphology, we conducted a comprehensive genetic and phenotypic analysis of in zebrafish, an emerging model for bone and mineral research.
View Article and Find Full Text PDFMutational analysis of an antimalarial drug target, ATP4.
Proc Natl Acad Sci U S A
January 2025
Department of Microbiology and Immunology, Center for Molecular Parasitology, Drexel University College of Medicine, Philadelphia, PA 19129.
Among new antimalarials discovered over the past decade are multiple chemical scaffolds that target P-type ATPase (ATP4). This essential protein is a Na pump responsible for the maintenance of Na homeostasis. ATP4 belongs to the type two-dimensional (2D) subfamily of P-type ATPases, for which no structures have been determined.
View Article and Find Full Text PDFRisk Factors Related to Resting Metabolic Rate-Related Gene Variation in Children with Overweight/Obesity: 3-Year Panel Study.
Nutrients
December 2024
Department of Food & Nutrition & Research Institute of Obesity Sciences, Sungshin Women's University, Dobongro-76gagil-55, Kangbuk-ku, Seoul 01133, Republic of Korea.
Unlabelled: This study investigated how the gene variation related to RMR alteration affects risk factors of obese environments in children with obesity aged 8-9.
Methods: Over a three-year follow-up period, 63.3% of original students participated.
Alleviating the Effects of Short QT Syndrome Type 3 by Allele-Specific Suppression of the Mutant Allele.
Int J Mol Sci
December 2024
Department of Medical Biology, Amsterdam Cardiovascular Sciences, Amsterdam University Medical Center, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands.
Short QT syndrome type 3 (SQTS3 or SQT3), which is associated with life-threatening cardiac arrhythmias, is caused by heterozygous gain-of-function mutations in the gene. This gene encodes the pore-forming α-subunit of the ion channel that carries the cardiac inward rectifier potassium current (I). These gain-of-function mutations either increase the amplitude of I or attenuate its rectification.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!