Longevity as a Complex Genetic Trait

Author(s):  
George L. Sutphin ◽  
Ron Korstanje
2018 ◽  
Vol 143 (6) ◽  
pp. 454-461 ◽  
Author(s):  
Xiaohong Wang ◽  
Bishun Ye ◽  
Xiangpeng Kang ◽  
Ting Zhou ◽  
Tongfei Lai

Tomato (Solanum lycopersicum) fruit ripening is a complex genetic trait correlating with notable fruit phenotypic, physiologic, and biochemical changes. Transcription factors (TFs) play crucial roles during this process. LeHB-1, an HD-zip homeobox protein, is a ripening-related TF and acts as an important regulator of fruit ripening. However, the detailed biochemical and molecular basis of LeHB-1 on tomato fruit ripening is unclear. In the current study, the biologic functions of LeHB-1 were determined by a potato virus X (PVX)-mediated gene-silencing approach. The results indicate that PVX-induced LeHB-1 silencing in tomato could decrease pigment accumulation and delay fruit ripening. Compared with controls, nonripening flesh retains a greater pH value and a lesser anthocyanin content. By evaluating expression levels of genes related to tomato fruit ripening, we inferred that LeHB-1 located at the downstream of LeMADS-RIN-mediated regulatory network. In addition, LeHB-1 silencing mainly disturbed phytoene desaturation and isomerization, and led to a decrease in trans-lycopene accumulation, but did not influence flavonoid biosynthesis directly in tomato fruit. The findings provide a theoretical foundation for illustrating the biologic functions of LeHB-1 in tomato fruit ripening and quality.


2005 ◽  
Vol 25 (18) ◽  
pp. 8311-8322 ◽  
Author(s):  
Bingzhong Xue ◽  
Ann Coulter ◽  
Jong Seop Rim ◽  
Robert A. Koza ◽  
Leslie P. Kozak

ABSTRACT Induction of brown adipocytes in white fat depots by adrenergic stimulation is a complex genetic trait in mice that affects the ability of the animal to regulate body weight. An 80-fold difference in expression of the mitochondrial uncoupling gene (Ucp1) at the mRNA and protein levels between A/J and C57BL/6J (B6) mice is controlled by allelic interactions among nine quantitative trait loci (QTLs) on eight chromosomes. Overlapping patterns of these QTLs also regulate expression levels of Pgc-1α, Pparα, and type 2 deiodinase. Independent validation that PPARα is associated with Ucp1 induction was obtained by treating mice with the PPARα agonist clofibrate, but not from the analysis of PPARα knockout mice. The most upstream sites of regulation for Ucp1 that differed between A/J and B6 were the phosphorylation of p38 mitogen-activated protein kinase and CREB and then followed by downstream changes in levels of mRNA for PPARγ, PPARα, PGC-1α, and type 2 deiodinase. However, compared to Ucp1 expression, the two- to fourfold differences in the expression of these regulatory components are very modest. It is proposed that small variations in the levels of several transcriptional components of the Ucp1 enhanceosome interact synergistically to achieve large differences in Ucp1 expression.


2002 ◽  
Vol 22 (2) ◽  
pp. 115-126 ◽  
Author(s):  
Friedrich C. Luft

2001 ◽  
Vol 21 (S1) ◽  
pp. S554-S559 ◽  
Author(s):  
Lars Beckmann ◽  
Christine Fischer ◽  
Klaus-Georg Deck ◽  
Ilja M. Nolte ◽  
Gerard te Meerman ◽  
...  

2010 ◽  
Vol 25 (5) ◽  
pp. 287-290 ◽  
Author(s):  
L.M. Fiori ◽  
G. Turecki

AbstractDespite strong evidence for a role of biological factors in the etiology and pathology of suicide, the study of traditional neurotransmitter systems has been able to explain only a small proportion of the neurobiology of what is now recognized as a complex genetic trait. The use of microarrays to simultaneously examine the expression levels of thousands of gene transcripts has vastly expanded our capacity to detect the involvement of additional genes and pathways in suicidality, and has opened many new avenues for the discovery of the biological underpinnings of suicide completion. This review examines microarray studies which have been used to identify genes displaying altered expression in suicide completers, and highlights some of the important methodological considerations and metabolic pathways which have emerged from these analyses.


1999 ◽  
Vol 17 (S1) ◽  
pp. S449-S459 ◽  
Author(s):  
David A. Greenberg ◽  
Jean W. Maccluer ◽  
M. Anne Spence ◽  
Catherine T. Falk ◽  
Susan E. Hodge

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