Table 1:

Summary of phenotypes associated with Sirtuin deficiency in oocytes

SIRTUIN	Mouse knockout models	Knockdown/Inhibition models
SIRT1	• Infertile • Impaired hypothalamic-pituitary-gonadal signaling	• Arrest at prophase I (∼50%) Chromosome and spindle abnormalities at MII (∼25%)
SIRT2	• Normal oocyte spindle assembly	• Reduced polar body extrusion rates (∼50%) • Poor and aberrant K-MT attachments in MI (50%) • Chromosome and spindle abnormalities at MII (∼35%) • Aneuploidy at MII (∼23%) • Increased H4K16ac and acetylated α-tubulin at MII
SIRT3	• Fertile • Normal oocyte meiotic maturation • Impaired in vitro embryo development after IVF • Increased ROS levels	• Normal oocyte meiotic maturation • Increased ROS levels
SIRT4	• N/A	• Normal oocyte meiotic maturation
SIRT5	• N/A	• N/A
SIRT6	• N/A	• Reduced polar body extrusion rates (∼40%) • Chromosome and spindle abnormalities at MI (∼27%) • Aberrant K-MT attachments at MI (50%) • Aneuploidy at MII (∼30%) • Increased H4K16ac in prophase I and MII
SIRT7	• Age dependent subfertility • Defects in chromosome synapsis during meiotic recombination • Reduced primordial follicle pool • Normal oocyte meiotic maturation • Aneuploidy at MII (∼50%)	• Reduced NEBD and polar body extrusion rates (~50%) • Chromosome and spindle abnormalities at MI (∼50%) • Enlarged polar body, symmetrical divisions and diminished actin cap at MII • Increased ROS levels and diminished ATP production • Impaired in vitro embryo development after IVF • Increased γH2Ax and apoptosis in early embryos