Opposite effects of stn1-L60F and stn1-ΔC on the HU sensitivity and checkpoint activation of mec1-100 cells.

(A) Exponentially growing cell cultures were serially diluted (1:10) and each dilution was spotted out onto YEPD plates with or without HU. (B) Cells were arrested in G1 with α-factor (time zero) and then released into YEPD containing 0.2M HU. Aliquots...

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Bibliografski detalji
Glavni autor:	Erika Casari (11432756) (author)
Daljnji autori:	Flavio Corallo (22439397) (author), Luca Edoardo Milani (22439400) (author), Renata Tisi (10153088) (author), Maria Pia Longhese (11432759) (author)
Izdano:	2025
Teme:	Biophysics Biochemistry Cell Biology Genetics Molecular Biology Science Policy Infectious Diseases Environmental Sciences not elsewhere classified Biological Sciences not elsewhere classified latter mechanism predominating function truncation (< function allele (< curb nuclease activity stalled replication forks ssdna ), yet restrain ssdna formation exposing replication forks div >< p cst subunit stn1 degradation </ p checkpoint kinases mec1 replication stress reduces ssdna nucleolytic degradation l60f </ c </ suppression exerted stranded dna stn1 works stn1 opposes stn1 -</ resection activities promoting polα nucleotide depletion dependent fill deficient cells >) suppresses >) exacerbates
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Opposite effects of <i>stn1-L60F</i> and <i>stn1-</i>Δ<i>C</i> on the HU sensitivity and checkpoint activation of <i>mec1-100</i> cells.

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