Selective Instability: Maternal Effort and the Evolution of Gene Activation and Deactivation Rates

2003 ◽  
Vol 9 (3) ◽  
pp. 317-326
Author(s):  
Carlo C. Maley ◽  
Stephen J. Tapscott

We previously used simulations of gene expression to demonstrate that rapid activation and deactivation rates stabilized outcomes in stochastic systems. We hypothesized that transient single allele inactivation of an autosomal gene during gametogenesis or very early embryogenesis could have a selective advantage if it permits the functional sampling of each allele and precludes committing maternal effort to an embryo with a deleterious mutation. To test this hypothesis, we simulated the evolution of gene expression activation and deactivation rates and imposed two different selective pressures on the populations: (a) late selection against individuals that cannot maintain a threshold level of gene product that occurs after the investment of maternal effort (i.e., after birth); or (b) early selection: in addition to late selection, maintenance of the gene product above a threshold level was necessary for early development prior to commitment of maternal effort. We found that the opportunity to save reproductive effort from early selection caused the evolution of higher deactivation rates and lower activation rates than in the late selection condition. Thus, we predict that in the special case where early selection can save maternal investment in non-viable offspring, gene expression activation rates and deactivation rates might be selected to permit sampling of the product from each allele.

2019 ◽  
Author(s):  
Khem Raj Ghusinga ◽  
Abhyudai Singh

AbstractAn important step in execution of several cellular processes is accumulation of a regulatory protein up to a specific threshold level. Since production of a protein is inherently stochastic, the time at which its level crosses a threshold exhibits cell-to-cell variation. A problem of interest is to characterize how the statistics of event timing is affected by various steps of protein expression. Our previous work studied this problem by considering a gene expression model where gene was always active. Here we extend our analysis to a scenario where gene stochastically switches between active and inactive states. We formulate event timing as the first-passage time for a protein’s level to cross a threshold and investigate how the rates of gene activation/inactivation affect the distribution and moments of the first-passage time. Our results show that both the time-scale of gene switching with respect to the protein degradation rate as well as the ratio of the gene inactivation to gene activation rates are important parameters in shaping the event-timing distribution.


1991 ◽  
Vol 11 (1) ◽  
pp. 55-62 ◽  
Author(s):  
M A Marshall ◽  
W E Timberlake

The Aspergillus nidulans wetA gene is required for synthesis of cell wall layers that make asexual spores (conidia) impermeable. In wetA mutant strains, conidia take up water and autolyze rather than undergoing the final stages of maturation. wetA is activated during conidiogenesis by sequential expression of the brlA and abaA regulatory genes. To determine whether wetA regulates expression of other sporulation-specific genes, its coding region was fused to a nutritionally regulated promoter that permits gene activation in vegetative cells (hyphae) under conditions that suppress conidiation. Expression of wetA in hyphae inhibited growth and caused excessive branching. It did not lead to activation of brlA or abaA but did cause accumulation of transcripts from genes that are normally expressed specifically during the late stages of conidiation and whose mRNAs are stored in mature spores. Thus, wetA directly or indirectly regulates expression of some spore-specific genes. At least one gene (wA), whose mRNA does not occur in spores but rather accumulates in the sporogenous phialide cells, was activated by wetA, suggesting that wetA may have a regulatory function in these cells as well as in spores. We propose that wetA is responsible for activating a set of genes whose products make up the final two conidial wall layers or direct their assembly and through this activity is responsible for acquisition of spore dormancy.


Chromosoma ◽  
2014 ◽  
Vol 123 (5) ◽  
pp. 481-489 ◽  
Author(s):  
Yuichiro Itoh ◽  
Arthur P. Arnold

2001 ◽  
Vol 1 ◽  
pp. 653-655 ◽  
Author(s):  
Jennifer E. Fox ◽  
Matthew E. Burow ◽  
John A. McLachlan

Endocrine disrupting chemicals (EDCs) include organochlorine pesticides, plastics manufacturing by-products, and certain herbicides[1]. These chemicals have been shown to disrupt hormonal signaling in exposed wildlife, lab animals, and mammalian cell culture by binding to estrogen receptors (ER-α and ER-β) and affecting the expression of estrogen responsive genes[2,3]. Additionally, certain plant chemicals, termed phytoestrogens, are also able to bind to estrogen receptors and modulate gene expression, and as such also may be considered EDCs[4]. One example of phytoestrogen action is genistein, a phytochemical produced by soybeans, binding estrogen receptors, and changing expression of estrogen responsive genes which certain studies have linked to a lower incidence of hormonally related cancers in Japanese populations[5]. Why would plants make compounds that are able to act as estrogens in the human body? Obviously, soybeans do not intentionally produce phytoestrogens to prevent breast cancer in Japanese women.


2020 ◽  
Vol 117 (48) ◽  
pp. 30805-30815
Author(s):  
Mingzhe Shen ◽  
Chae Jin Lim ◽  
Junghoon Park ◽  
Jeong Eun Kim ◽  
Dongwon Baek ◽  
...  

Transcriptional regulation is a complex and pivotal process in living cells. HOS15 is a transcriptional corepressor. Although transcriptional repressors generally have been associated with inactive genes, increasing evidence indicates that, through poorly understood mechanisms, transcriptional corepressors also associate with actively transcribed genes. Here, we show that HOS15 is the substrate receptor for an SCF/CUL1 E3 ubiquitin ligase complex (SCFHOS15) that negatively regulates plant immunity by destabilizing transcriptional activation complexes containing NPR1 and associated transcriptional activators. In unchallenged conditions, HOS15 continuously eliminates NPR1 to prevent inappropriate defense gene expression. Upon defense activation, HOS15 preferentially associates with phosphorylated NPR1 to stimulate rapid degradation of transcriptionally active NPR1 and thus limit the extent of defense gene expression. Our findings indicate that HOS15-mediated ubiquitination and elimination of NPR1 produce effects contrary to those of CUL3-containing ubiquitin ligase that coactivate defense gene expression. Thus, HOS15 plays a key role in the dynamic regulation of pre- and postactivation host defense.


2017 ◽  
Vol 47 (12) ◽  
Author(s):  
Mariana Batista Rodrigues Faleiro ◽  
Lorena Cardoso Cintra ◽  
Rosália Santos Amorim Jesuino ◽  
Eugênio Gonçalves de Araújo ◽  
Rafael Malagoli Rocha ◽  
...  

ABSTRACT: Gene expression of ErbB1 and ErbB2, and immunostaining of EGFR (Her1) and Her2 (c-erbB-2) were evaluated in this study to ascertain whether these receptors are involved in the evolution of canine premalignant and malignant prostatic lesions, as proliferative inflammatory atrophy (PIA) and prostatic carcinoma (PC). With regards to the intensity of EGFR immunostaining, there was no difference between normal prostatic tissue and tissues with PIA or PC. In relation to Her2 immunostaining, there were differences between normal prostatic tissue and those with PIA and PC, as also differences between prostates with PIA and PC. There was no correlation between EGFR and Her2 immunostaining. ErbB1 gene product was detected in two normal tissue samples, in one with PIA, and in all samples with PC. ErbB2 mRNA was recorded in two canine samples with PIA, in all with PC, but was not detected in normal prostatic tissue. It was concluded that EGFR and Her2 play roles in canine PIA and PC, suggesting that those receptors may be involved in canine prostatic carcinogenesis.


2015 ◽  
Author(s):  
Andrew C Bergen ◽  
Gerilyn M Olsen ◽  
Justin C Fay

Qualitative patterns of gene activation and repression are often conserved despite an abundance of quantitative variation in expression levels within and between species. A major challenge to interpreting patterns of expression divergence is knowing which changes in gene expression affect fitness. To characterize the fitness effects of gene expression divergence we placed orthologous promoters from eight yeast species upstream of malate synthase (MLS1) in Saccharomyces cerevisiae. As expected, we found these promoters varied in their expression level under activated and repressed conditions as well as in their dynamic response following loss of glucose repression. Despite these differences, only a single promoter driving near basal levels of expression caused a detectable loss of fitness. We conclude that the MLS1 promoter lies on a fitness plateau whereby even large changes in gene expression can be tolerated without a substantial loss of fitness.


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