期刊
BLOOD
卷 112, 期 4, 页码 1493-1502出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2008-02-137398
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- NCI NIH HHS [R01 CA105463, R01 CA099179] Funding Source: Medline
- NHLBI NIH HHS [K08 HL084199] Funding Source: Medline
- NIDDK NIH HHS [R21 DK074519, R21 DK074519-02, R21 DK074519-01] Funding Source: Medline
Production of a red blood cell's hemoglobin depends on mitochondrial heme synthesis. However, mature red blood cells are devoid of mitochondria and rely on glycolysis for ATP production. The molecular basis for the selective elimination of mitochondria from mature red blood cells remains controversial. Recent evidence suggests that clearance of both mitochondria and ribosomes, which occurs in reticulocytes following nuclear extrusion, depends on aurtophagy. Here, we demonstrate that Ulk1, a serine threonine kinase with homology to yeast atg1 p, is a critical regulator of mitochondrial and ribosomal clearance during the final stages of erythroid maturation. However, in contrast to the core autophagy genes such as atg5 and atg7, expression of ulk1 is not essential for induction of macroautophagy in response to nutrient deprivation or for survival of newborn mice. Together, these data suggest that the ATG1 homologue, Ulk1, is a component of the selective autophagy machinery that leads to the elimination of organelles in erythroid cells rather that an essential mechanistic component of autophagy.
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