Robert Wysocki

Robert Wysocki – polski biolog molekularny, genetyk i mikrobiolog; prof. dr hab. nauk biologicznych, dyrektor i profesor nadzwyczajny Instytutu Biologii Eksperymentalnej, oraz Instytutu Genetyki i Mikrobiologii Wydziału Nauk Biologicznych Uniwersytetu Wrocławskiego.

Robert Wysocki

Państwo działania	Polska
profesor nauk biologicznych
Specjalność: genetyka, mikrobiologia
Doktorat	24 czerwca 1999
Habilitacja	6 października 2005
Profesura	7 sierpnia 2012

Życiorys

24 czerwca 1999 obronił pracę doktorską Struktura i funkcja genów ACR3 i ACR2 warunkujących oporność komórek drożdży Saccharomyces cerevisiae na sole arsenu, otrzymując doktorat, a 6 października 2005 habilitował się na podstawie oceny dorobku naukowego i pracy zatytułowanej Mechanizmy tolerancji komórek drożdży Saccharomyces cerevisiae na arsen i antymon. 7 sierpnia 2012 nadano mu tytuł profesora w zakresie nauk biologicznych.

Został zatrudniony na stanowisku dyrektora i profesora nadzwyczajnego w Instytucie Biologii Eksperymentalnej, oraz w Instytucie Genetyki i Mikrobiologii na Wydziale Nauk Biologicznych Uniwersytetu Wrocławskiego.

Wybrane publikacje naukowe

• Structure of E69Q mutant of human muscle fructose-1,6-bisphosphatase
• Functional characterization of the S. cerevisiae genome by gene deletion and parallel analysis
• The yeast aquaglyceroporin Fps1p is a bidirectional arsenite channel.
• Transcriptional activation of metalloid tolerance genes in Saccharomyces cerevisiae requires the AP-1-like proteins Yap1p and Yap8p.
• The yeast permease Acr3p is a dual arsenite and antimonite plasma membrane transporter.
• The MAPK Hog1p modulates Fps1p-dependent arsenite uptake and tolerance in yeast.
• CDK Pho85 targets CDK inhibitor Sic1 to relieve yeast G1 checkpoint arrest after DNA damage.
• Multiple cysteine residues are necessary for sorting and transport activity of the arsenite permease Acr3p from Saccharomyces cerevisiae.
• Yeast G1 DNA damage checkpoint regulation by H2A phosphorylation is independent of chromatin remodeling
• Role of Dot1-dependent histone H3 methylation in G1 and S phase DNA damage checkpoint functions of Rad9.
• Characterization of the DNA-binding motif of the arsenic-responsive transcription factor Yap8p.
• Acr3p is a plasma membrane antiporter that catalyzes As(III)/H(+) and Sb(III)/H(+) exchange in Saccharomyces cerevisiae.
• Design, synthesis, and characterization of a highly effective Hog1 inhibitor: a powerful tool for analyzing MAP kinase signaling in yeast
• Oxidative stress and replication-independent DNA breakage induced by arsenic in Saccharomyces cerevisiae
• Disentangling genetic and epigenetic determinants of ultrafast adaptation
• The YJL185C, YLR376C and YJR129C genes of Saccharomyces cerevisiae are probably involved in regulation of the glyoxylate cycle.
• The LSH/HELLS homolog Irc5 contributes to cohesin association with chromatin in yeast
• Arsenic and antimony transporters in eukaryotes
• Yeast cell death during DNA damage arrest is independent of caspase or reactive oxygen species.
• How Saccharomyces cerevisiae copes with toxic metals and metalloids.
• Different sensitivities of mutants and chimeric forms of human muscle and liver fructose-1,6-bisphosphatases towards AMP.
• The Swi2-Snf2-like protein Uls1 is involved in replication stress response.
• New insights into cohesin loading.
• Transmembrane topology of the arsenite permease Acr3 from Saccharomyces cerevisiae.
• Mitogen-activated protein kinase Hog1 mediates adaptation to G1 checkpoint arrest during arsenite and hyperosmotic stress.
• The mitogen-activated protein kinase Slt2 modulates arsenite transport through the aquaglyceroporin Fps1.
• Metalloid tolerance based on phytochelatins is not functionally equivalent to the arsenite transporter Acr3p.
• The genetic characteristics Saccharomyces cerevisiae aci(+) mutants.
• Swi2/Snf2-like protein Uls1 functions in the Sgs1-dependent pathway of maintenance of rDNA stability and alleviation of replication stress.
• DNA Damage Tolerance Pathway Choice Through Uls1 Modulation of Srs2 SUMOylation in Saccharomyces cerevisiae.
• Identification of critical residues for transport activity of Acr3p, the Saccharomyces cerevisiae As(III)/H+ antiporter.
• Arsenical resistance genes in Saccharomyces douglasii and other yeast species undergo rapid evolution involving genomic rearrangements and duplications.
• Mass-murdering: deletion of twenty-three ORFs from Saccharomyces cerevisiae chromosome XI reveals five genes essential for growth and three genes conferring detectable mutant phenotype
• Error-free DNA damage tolerance pathway is facilitated by the Irc5 translocase through cohesin
• Elucidating the response of Kluyveromyces lactis to arsenite and peroxide stress and the role of the transcription factor KlYap8
• Mechanisms of toxic metal tolerance in yeast
• Yap1 overproduction restores arsenite resistance to the ABC transporter deficient mutant ycf1 by activating ACR3 expression
• The Emerging Role of Cohesin in the DNA Damage Response
• The ancillary N-terminal region of the yeast AP-1 transcription factor Yap8 contributes to its DNA binding specificity
• Coupling of RNA polymerase III assembly to cell cycle progression in Saccharomyces cerevisiae
• Rsp5-dependent endocytosis and degradation of the arsenite transporter Acr3 requires its N-terminal acidic tail as an endocytic sorting signal and arrestin-related ubiquitin-ligase adaptors
• Arsenic and Yeast Aquaglyceroporin
• Saccharomyces cerevisiae as a Model Organism for Elucidating Arsenic Tolerance Mechanisms