scholarly journals Mammalian Septins Nomenclature

2002 ◽  
Vol 13 (12) ◽  
pp. 4111-4113 ◽  
Author(s):  
Ian G. Macara ◽  
Richard Baldarelli ◽  
Christine M. Field ◽  
Michael Glotzer ◽  
Yasuhide Hayashi ◽  
...  
Keyword(s):  
Human Genome ◽  
Gene Product ◽  
Genome Organization ◽  
Splice Variants ◽  
Gene Products ◽  
Gene Nomenclature ◽  
Nomenclature System ◽  
Nomenclature Committee ◽  
Human And Mouse ◽  
Mouse Genomic

There are 10 known mammalian septin genes, some of which produce multiple splice variants. The current nomenclature for the genes and gene products is very confusing, with several different names having been given to the same gene product and distinct names given to splice variants of the same gene. Moreover, some names are based on those of yeast or Drosophilaseptins that are not the closest homologues. Therefore, we suggest that the mammalian septin field adopt a common nomenclature system, based on that adopted by the Mouse Genomic Nomenclature Committee and accepted by the Human Genome Organization Gene Nomenclature Committee. The human and mouse septin genes will be namedSEPT1–SEPT10 and Sept1–Sept10, respectively. Splice variants will be designated by an underscore followed by a lowercase “v” and a number, e.g., SEPT4_v1.

scholarly journals Myosin-I nomenclature

2001 ◽  
Vol 155 (5) ◽  
pp. 703-704 ◽  
Author(s):  
Peter G. Gillespie ◽  
Joseph P. Albanesi ◽  
Martin Bähler ◽  
William M. Bement ◽  
Jonathan S. Berg ◽  
...  
Keyword(s):  
Human Genome ◽  
Genome Organization ◽  
Genome Annotation ◽  
Nomenclature System ◽  
Myosin I

We suggest that the vertebrate myosin-I field adopt a common nomenclature system based on the names adopted by the Human Genome Organization (HUGO). At present, the myosin-I nomenclature is very confusing; not only are several systems in use, but several different genes have been given the same name. Despite their faults, we believe that the names adopted by the HUGO nomenclature group for genome annotation are the best compromise, and we recommend universal adoption.

scholarly journals The immunosuppressant SR 31747 blocks cell proliferation by inhibiting a steroid isomerase in Saccharomyces cerevisiae.

1996 ◽  
Vol 16 (6) ◽  
pp. 2719-2727 ◽  
Author(s):  
S Silve ◽  
P Leplatois ◽  
A Josse ◽  
P H Dupuy ◽  
C Lanau ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Proliferation ◽  
Gene Product ◽  
In Vitro Assays ◽  
Gene Products ◽  
Yeast Saccharomyces Cerevisiae ◽  
Isomerase Activity ◽  
Encoding Gene ◽  
Resistant Mutants

SR 31747 is a novel immunosuppressant agent that arrests cell proliferation in the yeast Saccharomyces cerevisiae, SR 31747-treated cells accumulate the same aberrant sterols as those found in a mutant impaired in delta 8- delta 7-sterol isomerase. Sterol isomerase activity is also inhibited by SR 31747 in in vitro assays. Overexpression of the sterol isomerase-encoding gene, ERG2, confers enhanced SR resistance. Cells growing anaerobically on ergosterol-containing medium are not sensitive to SR. Disruption of the sterol isomerase-encoding gene is lethal in cells growing in the absence of exogenous ergosterol, except in SR-resistant mutants lacking either the SUR4 or the FEN1 gene product. The results suggest that sterol isomerase is the target of SR 31747 and that both the SUR4 and FEN1 gene products are required to mediate the proliferation arrest induced by ergosterol depletion.

Deletions in the C-terminal coding region of the v-sis gene: dimerization is required for transformation

1986 ◽  
Vol 6 (4) ◽  
pp. 1304-1314
Author(s):  
M Hannink ◽  
M K Sauer ◽  
D J Donoghue
Keyword(s):  
Growth Factor ◽  
Gene Product ◽  
Platelet Derived Growth Factor ◽  
Deletion Mutants ◽  
Gene Products ◽  
Coding Region ◽  
Strong Connection ◽  
C Terminus ◽  
Its Gene ◽  
Transforming Gene

The v-sis gene encodes chain B of platelet-derived growth factor. However, this gene codes for additional amino acids at both the N terminus and the C terminus of its gene product which are not present in the amino acid sequence of platelet-derived growth factor. We constructed a series of deletion mutants with deletions in the v-sis gene in order to define the C-terminal limit of the v-sis gene product which is required for transformation. Deletion mutants of the v-sis gene which encoded truncated gene products up to 57 residues shorter than the v-siswt gene product were still able to transform cells. The minimal transforming region of the v-sis gene product contained six residues fewer than were present in chain B of platelet-derived growth factor. Only 10 residues, including the sequence Cys-Lys-Cys, separated the smallest transforming gene product from the largest nontransforming gene product. These cysteine residues were also important for dimerization of the v-sis gene product, since all of the nontransforming v-sis deletions were unable to form dimers when they were analyzed under nonreducing conditions. Our results suggest that there is a strong connection between transformation and dimerization.

Novel conserved elements upstream of theH19gene are transcribed and act as mesodermal enhancers

Development ◽  
2002 ◽  
Vol 129 (5) ◽  
pp. 1205-1213
Author(s):  
Robert A. Drewell ◽  
Katharine L. Arney ◽  
Takahiro Arima ◽  
Sheila C. Barton ◽  
James D. Brenton ◽  
...  
Keyword(s):  
Gene Expression ◽  
Expression Pattern ◽  
Reporter Gene ◽  
Differentially Methylated Region ◽  
Genomic Sequencing ◽  
Strong Homology ◽  
Imprinting Control Region ◽  
Enhancer Function ◽  
Human And Mouse ◽  
Mouse Genomic

The reciprocally imprinted H19 and Igf2 genes form a co-ordinately regulated 130 kb unit in the mouse controlled by widely dispersed enhancers, epigenetically modified silencers and an imprinting control region (ICR). Comparative human and mouse genomic sequencing between H19 and Igf2 revealed two novel regions of strong homology upstream of the ICR termed H19 upstream conserved regions (HUCs). Mouse HUC1 and HUC2 act as potent enhancers capable of driving expression of an H19 reporter gene in a range of mesodermal tissues. Intriguingly, the HUC sequences are also transcribed bi-allelically in mouse and human, but their expression pattern in neural and endodermal tissues in day 13.5 embryos is distinct from their enhancer function. The location of the HUC mesodermal enhancers upstream of the ICR and H19, and their capacity for interaction with both H19 and Igf2 requires critical re-evaluation of the cis-regulation of imprinted gene expression of H19 and Igf2 in a range of mesodermal tissues. We propose that these novel sequences interact with the ICR at H19 and the epigenetically regulated silencer at differentially methylated region 1 (DMR1) of Igf2.

Molecular Insights into Regulation of L-Type Ca Channel Function

Physiology ◽  
1991 ◽  
Vol 6 (6) ◽  
pp. 277-281 ◽  
Author(s):  
P Lory ◽  
G Varadi ◽  
A Schwartz
Keyword(s):  
Structure Function ◽  
Splice Variants ◽  
Ca Channel ◽  
Gene Products ◽  
Ca Channels ◽  
Channel Activity ◽  
Excitable Cells ◽  
Multiple Gene ◽  
Channel Function ◽  
Voltage Dependent

The diversity of voltage-dependent Ca channels is well documented. How excitable cells produce their specific Ca channel activity is being approached by structure-function studies. The implications of multiple gene products, splice variants, and subunit assembly in Ca channel function are updated in this review.

scholarly journals Conserved genomic neighborhood is a strong but no perfect indicator for a direct interaction of microbial gene products

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Robert Esch ◽  
Rainer Merkl
Keyword(s):  
Gene Product ◽  
Protein Complexes ◽  
Sequence Similarity ◽  
False Positive Rate ◽  
Direct Interaction ◽  
Interaction Partner ◽  
Gene Products ◽  
Genomic Context ◽  
Positive Rate ◽  
Genomic Neighborhood

Abstract Background The order of genes in bacterial genomes is not random; for example, the products of genes belonging to an operon work together in the same pathway. The cotranslational assembly of protein complexes is deemed to conserve genomic neighborhoods even stronger than a common function. This is why a conserved genomic neighborhood can be utilized to predict, whether gene products form protein complexes. Results We were interested to assess the performance of a neighborhood-based classifier that analyzes a large number of genomes. Thus, we determined for the genes encoding the subunits of 494 experimentally verified hetero-dimers their local genomic context. In order to generate phylogenetically comprehensive genomic neighborhoods, we utilized the tools offered by the Enzyme Function Initiative. For each subunit, a sequence similarity network was generated and the corresponding genome neighborhood network was analyzed to deduce the most frequent gene product. This was predicted as interaction partner, if its abundance exceeded a threshold, which was the frequency giving rise to the maximal Matthews correlation coefficient. For the threshold of 16%, the true positive rate was 45%, the false positive rate 0.06%, and the precision 55%. For approximately 20% of the subunits, the interaction partner was not found in a neighborhood of ± 10 genes. Conclusions Our phylogenetically comprehensive analysis confirmed that complex formation is a strong evolutionary factor that conserves genome neighborhoods. On the other hand, for 55% of the cases analyzed here, classification failed. Either, the interaction partner was not present in a ± 10 gene window or was not the most frequent gene product.

scholarly journals Silent rain: does the atmosphere-mediated connectivity between microbiomes influence bacterial evolutionary rates?

2020 ◽  
Vol 96 (7) ◽  
Author(s):  
Matti Jalasvuori
Keyword(s):  
Microbial Communities ◽  
Gene Product ◽  
Genetic Divergence ◽  
Epistatic Interaction ◽  
Genetic Material ◽  
Evolutionary Rates ◽  
Gene Products ◽  
Vast Number ◽  
Number Of Bacteria

ABSTRACT Air carries a vast number of bacteria and viruses over great distances all the time. This leads to continuous introduction of foreign genetic material to local, established microbial communities. In this perspective, I ask whether this silent rain may have a slowing effect on the overall evolutionary rates in the microbial biosphere. Arguably, the greater the genetic divergence between gene ‘donors’ and ‘recipients’, the greater the chance that the gene product has a deleterious epistatic interaction with other gene products in its genetic environment. This is due to the long-term absence of check for mutual compatibility. As such, if an organism is extensively different from other bacteria, genetic innovations are less probable to fit to the genome. Here, genetic innovation would be anything that elevates the fitness of the gene vehicle (e.g. bacterium) over its contemporaries. Adopted innovations increase the fitness of the compatible genome over incompatible ones, thus possibly tempering the pace at which mutations accumulate in existing genomes over generations. I further discuss the transfer of bacteriophages through atmosphere and potential effects that this may have on local dynamics and perhaps phage survival.

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