Dihydroxyacetone production from methanol by a dihydroxyacetone kinase deficient mutant of Hansenula polymorpha

1986 ◽  
Vol 23 (3-4) ◽  
Author(s):  
Nobuo Kato ◽  
Hisataka Kobayashi ◽  
Masayuki Shimao ◽  
Chikahiro Sakazawa
Keyword(s):  
Hansenula Polymorpha ◽  
Deficient Mutant ◽  
Dihydroxyacetone Kinase

Dihydroxyacetone kinase from a methylotrophic yeast, Hansenula polymorpha CBS 4732

1988 ◽  
Vol 150 (2) ◽  
pp. 155-159 ◽  
Author(s):  
Nobuo Kato ◽  
Hiroshi Yoshikawa ◽  
Katsuhiko Tanaka ◽  
Masayuki Shimao ◽  
Chikahiro Sakazawa
Keyword(s):  
Hansenula Polymorpha ◽  
Methylotrophic Yeast ◽  
Dihydroxyacetone Kinase

scholarly journals The Hansenula polymorpha per6 mutant is affected in two adjacent genes which encode dihydroxyacetone kinase and a novel protein, Pak1p, involved in peroxisome integrity

1998 ◽  
Vol 34 (1) ◽  
pp. 1-11 ◽  
Author(s):  
I. J. van der Klei ◽  
Meis van der Heide ◽  
Richard J. S. Baerends ◽  
Karl-Bj�rn Rechinger ◽  
Klaas Nicolay ◽  
...  
Keyword(s):  
Hansenula Polymorpha ◽  
Dihydroxyacetone Kinase ◽  
Novel Protein

scholarly journals Peroxisome reintroduction in Hansenula polymorpha requires Pex25 and Rho1

2011 ◽  
Vol 193 (5) ◽  
pp. 885-900 ◽  
Author(s):  
Ruchi Saraya ◽  
Arjen M. Krikken ◽  
Marten Veenhuis ◽  
Ida J. van der Klei
Keyword(s):  
Mutant Strain ◽  
De Novo ◽  
Hansenula Polymorpha ◽  
Protein Family ◽  
Yeast Cells ◽  
Deficient Mutant ◽  
Wild Type ◽  
Double Deletion ◽  
Insight Into

We identified two proteins, Pex25 and Rho1, which are involved in reintroduction of peroxisomes in peroxisome-deficient yeast cells. These are, together with Pex3, the first proteins identified as essential for this process. Of the three members of the Hansenula polymorpha Pex11 protein family—Pex11, Pex25, and Pex11C—only Pex25 was required for reintroduction of peroxisomes into a peroxisome-deficient mutant strain. In peroxisome-deficient pex3 cells, Pex25 localized to structures adjacent to the ER, whereas in wild-type cells it localized to peroxisomes. Pex25 cells were not themselves peroxisome deficient but instead contained a slightly increased number of peroxisomes. Interestingly, pex11 pex25 double deletion cells, in which both peroxisome fission (due to the deletion of PEX11) and reintroduction (due to deletion of PEX25) was blocked, did display a peroxisome-deficient phenotype. Peroxisomes reappeared in pex11 pex25 cells upon synthesis of Pex25, but not of Pex11. Reintroduction in the presence of Pex25 required the function of the GTPase Rho1. These data therefore provide new and detailed insight into factors important for de novo peroxisome formation in yeast.

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