Factors

We need to know every factor which determines lifespan.

Lifespan factors often but not always originate from defined genetic elements. They are not just genes, by definition they can be anything for which a Classifications schema can be build for that is related to the regulation of lifespan, such entities may include Single-Nucleotide Polymorphism, transcript variants, proteins and their complexes, compounds (i.e. small molecules like metabolites and drugs), etc. A factor should be based on a defined molecular entity or genomic position and been classified. It shall be highly flexible and scalable Concept.

While individual lifespan factors within each species or precise defined molecular entities will be captured within the Lifespan App, Data Entries of the Data App may summarize for instance the relevance of each factor class (e.g. homologous group; chemical derivate of related structure and properties, etc.) as well as draw overall conclusions. o

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  • symbol name observation species
    PLD alpha Antisense suppression of PLD alpha retards abscisic acid- and ethylene-induced senescence. Leaves detached from PLD alpha-deficient transgenic plants when inbutated in abscisic acid and ethylene exhibit a slower rate of senescence that those from wild-type and transgenic controls. PLD alpha deficient strains are associated with retardation of senescence as evidenced by delayed leaf yellowing, lower ion leakage, greater photosynthetic activity, and higher content of cholorophyl and phospholipids [9437863]. Antisense suppression of PLD alpha does not affect natural plant growth and development [9437863].
    SAG101 senescence-associated protein 101 Antisense RNA interference of SAG101 in transgenic plants delays the onset of leaf senescence for approximately 4 days, whereas chemical induced overexpression of SAG101 causes precocious senescence in both attached and detached leaves of transgenic plants [11971136].
    WRKY6 WRKY transcription factor 6 Deletion of the WRKY6 promoter results in defects in root and leaf cell senescence [11722756]. WRKY6 is a transcription factor involved in controlling processes related to senescence and pathogen defence [11722756] and is a positive regulator of PR1 expression [12000796]. WRKY6 is strongly expressed during senescence [11722756].
    pka1 cAMP-dependent protein kinase 1 pka1 knockouts exhibits a three-fold increase in chronological lifespan with up to 187% longer maximum lifespan [16822282]. Deleting ser/thr cAMP-activated protein kinase pka1 extends chronological lifespan under normal condition, but there is no additive effect with DR [20075862]. Fission yeast
    SAM1 S-adenosylmethionine synthetase, catalyzes transfer of the adenosyl group of ATP to the sulfur atom of methionine; one of two differentially regulated isozymes (Sam1p and Sam2p) Deletion of SAM1 increases replicative lifespan by 20% in the alpha strain and 15% in the a strain [18340043]. Budding yeast
    CKA2 CK2 subunit 2 CKA2 deletion approximately doubles mean chronological lifespan under starvation/extreme DR in BY4741 also increases as well as as heat-shock resistance in SDC medium in the W303-1A and DBY746 genetic backgrounds [20657825]. Budding yeast
    CKB2 Casein Kinase Beta' subunit Lack of Ckb2 promotes a modest but significant chronological lifespan extension and marked increase in yeat resistance [20657825]. Budding yeast
    CUP9 Homeodomain-containing transcriptional repressor of PTR2, which encodes a major peptide transporter; imported peptides activate ubiquitin-dependent proteolysis, resulting in degradation of Cup9p and de-repression of PTR2 transcription Deletion of CUP9 increases replicative lifespan by 30% in the alpha and a strains [18340043]. Although CPU9 was identified as a potential long-lived mutant strain in a bar-code screen, the chronological lifespan of CUP9 deletion mutant is not significantly different from than of wild-type under starvation/extreme DR [20657825]. Budding yeast
    TRM9 TRna Methyltransferase 9 TRM9 deletion almost triples mean chronological lifespan under starvation/extreme DR, increases heat resistance, but reduces resistance to acetic acid. Similar effect were present in the BY746 background in SDC medium [20657825]. Budding yeast
    RPL12B Ribosomal Protein of the Large subunit 12B Deletion of RPL12B increases mean replicative lifespan by 20% in the alpha strain [18423200] and by 22% in the remade strain, but increases non-significantly the mean replicative lifespan by 13% in the ORF collection [22377630]. RPL12B mutation promotes mean chronological longevity extension and heat-shock resistance but reduces acetic acid resistance under starvation/extreme DR. In DBY746 mutation of RPL12B almost doubles mean chronological lifespan in SDC medium and increases heat-shock resistance [20657825] Budding yeast
    PMR1 High affinity Ca2+/Mn2+ P-type ATPase required for Ca2+ and Mn2+ transport into Golgi; involved in Ca2+ dependent protein sorting and processing; mutations in human homolog ATP2C1 cause acantholytic skin condition Hailey-Hailey disease Deletion of PMR1 increses the replicative lifespan by 40% in the alpha strain and by 15% in the a strain. Overexpression of PMR1 extends the lifespan [21918615]. Budding yeast
    BRE5 BREfeldin A sensitivity 5 Deletion of BRE5 increases mean replicative lifespan by 30% [16293764] and mean chronological lifespan in diploid cells [21447998] Budding yeast
    CCR4 Carbon Catabolite Repression 4 Deletion of CCR4 increases mean chronological lifespan by 20 - 41% (20, 33, 41) in diploid cells [21447998]. In W303R CCR4 deletion shortens replicative lifespan by approximately 80% and results in temperature sensitivity that is suppressed by SSD1-V. SSD1-V partially suppresses the short-lifespan of ccr4 mutant. CCR4 mutation is synthetically lethal in combination with deletion of MPT5 in the absence of SSD1-V [11805047]. Budding yeast
    CDC6 Cell Division Cycle The CDC6-1 conditional allele results in an approximately 20% increase in mean replicative life span. This allele is defective for replicative initiation form the rDNA ARS at 27 degree Celsius, resulting in a reduced rate of extrachromosomal rDNA circle accumulation [9428525]. The cdc6-1 allele results in genomic instability at the permissive temperature [8552037]. Budding yeast
    GPA2 G Protein Alpha subunit 2 Deletion of GPA2 increases mean and maximum replicative lifespan by 40% and 26%, respectively [11000115]. Deletion of GPA2 extends replicative lifespan by reducing cAMP-PKA activity and provides a genetic model for DR [11000115]. Budding yeast
    DNM1 Dnm1p Deletion of DNM1 extends significantly mean and maximum lifespan by 49 and 111% in FY10 strain and by 15 and 12% in BY4741 strain [17173038]. Budding yeast
    RAS1 Deletion in RAS1 increases mean (23%) and maximum (29%) replicative lifespan (in SP1) [8034612]. RAS1 deletion increases replicative lifespan by 15% in the alpha strain [19030232]. However, deletion of RAS1 slightly shortens chronological lifespan (in SP1) [12586694]. No lifespan extension results from overexpression of RAS1 (in SP1) [8034612]. Budding yeast
    REI1 Cytoplasmic pre-60S factor REI1 deletion increases mean replicative lifespan by about 40% [16293764] in the alpha and a strains [19030232]. Budding yeast
    ROM2 RhO1 Multicopy suppressor 2 Deletion of ROM2 increases mean replicative lifespan of the alpha strain by about 50% [16293764]. ROM deletion mutant replicative lifespan increases by 49% in the alpha strain and 16% in a strain. Deletion of ROM2 increases replicative lifespan by 38% in the alpha strain and by 29.3% in the a strain (34.2% in both) [19030232]. Budding yeast
    RPL6B Ribosomal Protein of the Large subunit 6B Deletion of RPL6B significantly increases replicative lifespan [17174052]. Replicative lifespan increases by 15% in the alpha strain and 30-40% in a strain [19030232; 18340043; 18423200]. RPL6B deletion increases replicative lifespan by 30% [16293764]. Budding yeast
    SCP1 S. cerevisiae CalPonin 1 Increasing actin dynamics by deletion of SCP1, encoding an actin bundling protein, increases replicative lifespan by 67% as well as chronological lifespan by 88%, whereas its overexpression leads to elevuated ROS levels and reduces chronological lifespan (in KAY446 strain) [15024029]. SCP1 is related to mammalian SM22/transgelin which is induced during senescence [9570922]. Budding yeast
    SSD1 Suppressor of SIT4 Deletion 1 Overexpression of SSD1 (addition of a SSD1-V allele) increases replicative lifespan by 50%, independently of SIR2 and SIR2 further extends the lifespan, although SIR2 is necessary for SSD1-V cells to attain maximal lifespan [15126388]. SSD1-V also dramatically increases chronological lifespan with lifespan twice as long as ssd1-d cells [19570907]. Deletion of SSD1 increases replicative lifespan by 50% [Li et al., 2009]. Addition of SSD1-V allele to an ssd1-d strain suppresses the short lifespan of an MPT5 deletion mutant [11805047] and extend wild-type lifespan [Kaeberlein and Guarente, unpublished]. SSD1-V slightly extends the lifespan of swi4 and ccr4 mutant strains and suppresses the temperature sensitive growth phenotype of mpt5, ccr3, swi4, and swi6 single mutants [11805047]. SSD1-V also suppresses the synthetic lethality caused by deletion of MPT5 in combination with a mutation in SWI4, SWI6, or CCR4 [11805047]. SSD1-V suppresses mutations that affect cell wall stability [1545797; 8386319], RNA polymerase III activity [8510644], RNA splicing [10446233], and PKA activity [1848673; 8200529]. Budding yeast
    URE2 UREidosuccinate transport 2 Deletion of URE2 increase mean replicative lifespan by 21-31% in BY4742 [16293764]. URE2 deletion increases replicative lifespan increased by 20% in the alpha strain [19030232]. Budding yeast
    YBR238C Deletion of YBR238C increases mean replicative lifespan by 25 to 34% in the alpha and a strains [16293764; 19030232]. Budding yeast
    CPR7 Cyclosporin-sensitive Proline Rotamase 7 Deletion of CPR7 has no effect on lifespan replicative lifespan, but increases chronological lifespan [11361336] Budding yeast
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    • 25 of 456 factors
    Factors are an extension of GenAge and GenDR.

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