Keyword search (4,163 papers available)

"Lam A" Authored Publications:

Title Authors PubMed ID
1 The Adr1 transcription factor directs regulation of the ergosterol pathway and azole resistance in Candida albicans Shrivastava M; Kouyoumdjian GS; Kirbizakis E; Ruiz D; Henry M; Vincent AT; Sellam A; Whiteway M; 37791798
BIOLOGY
2 Trauma-informed Approaches to Substance Use Interventions with Indigenous Peoples: A Scoping Review Pride T; Lam A; Swansburg J; Seno M; Lowe MB; Bomfim E; Toombs E; Marsan S; LoRusso J; Roy J; Gurr E; LaFontaine J; Paul J; Burack JA; Mushquash C; Stewart SH; Wendt DC; 34895091
PSYCHOLOGY
3 Loss of Arp1, a putative actin-related protein, triggers filamentous and invasive growth and impairs pathogenicity in Candida albicans. Yao S, Feng Y, Islam A, Shrivastava M, Gu H, Lu Y, Sheng J, Whiteway M, Feng J 33363697
BIOLOGY
4 The Canadian Fungal Research Network: current challenges and future opportunities. Horianopoulos LC, Gluck-Thaler E, Benoit Gelber I, Cowen LE, Geddes-McAlister J, Landry CR, Schwartz IS, Scott JA, Sellam A, Sheppard DC, Spribille T, Subramaniam R, Walker AK, Harris SD, Shapiro RS, Gerstein A 32717148
BIOLOGY
5 Hof1 plays a checkpoint related role in MMS induced DNA damage response in Candida albicans. Feng J, Islam A, Bean B, Feng J, Sparapani S, Shrivastava M, Goyal A, Omran RP, Mallick J, Whiteway M 31940254
BIOLOGY
6 The Genomic Landscape of the Fungus-Specific SWI/SNF Complex Subunit, Snf6, in Candida albicans. Tebbji F, Chen Y, Sellam A, Whiteway M 29152582
BIOLOGY
7 Integration of Growth and Cell Size via the TOR Pathway and the Dot6 Transcription Factor in Candida albicans. Chaillot J, Tebbji F, Mallick J, Sellam A 30593490
BIOLOGY
8 Functional divergence of a global regulatory complex governing fungal filamentation. Polvi EJ, Veri AO, Liu Z, Hossain S, Hyde S, Kim SH, Tebbji F, Sellam A, Todd RT, Xie JL, Lin ZY, Wong CJ, Shapiro RS, Whiteway M, Robbins N, Gingras AC, Selmecki A, Cowen LE 30615616
BIOLOGY
9 Mms21: A Putative SUMO E3 Ligase in Candida albicans That Negatively Regulates Invasiveness and Filamentation, and Is Required for the Genotoxic and Cellular Stress Response. Islam A, Tebbji F, Mallick J, Regan H, Dumeaux V, Omran RP, Whiteway M 30530734
PERFORM

 

Title:Integration of Growth and Cell Size via the TOR Pathway and the Dot6 Transcription Factor in Candida albicans.
Authors:Chaillot JTebbji FMallick JSellam A
Link:https://www.ncbi.nlm.nih.gov/pubmed/30593490?dopt=Abstract
DOI:10.1534/genetics.118.301872
Publication:Genetics
Keywords:cell divisioncell growthcell sizeribosome biogenesistranscriptional rewiring
PMID:30593490 Category:Genetics Date Added:2019-06-07
Dept Affiliation: BIOLOGY
1 Centre hospitalier Universitaire de Québec (CHUQ) Research Center, Université Laval, Quebec G1V 4G2, Canada.
2 Department of Biology, Concordia University, Montréal, Quebec H3G 1M8, Canada.
3 Centre hospitalier Universitaire de Québec (CHUQ) Research Center, Université Laval, Quebec G1V 4G2, Canada adnane.sellam.1@ulaval.ca.
4 Department of Microbiology, Infectious Disease and Immunology, Faculty of Medicine, Université Laval, Quebec G1V 4G2, Canada.

Description:

Integration of Growth and Cell Size via the TOR Pathway and the Dot6 Transcription Factor in Candida albicans.

Genetics. 2019 02;211(2):637-650

Authors: Chaillot J, Tebbji F, Mallick J, Sellam A

Abstract

In most species, size homeostasis appears to be exerted in late G1 phase as cells commit to division, called Start in yeast and the Restriction Point in metazoans. This size threshold couples cell growth to division, and, thereby, establishes long-term size homeostasis. Our former investigations have shown that hundreds of genes markedly altered cell size under homeostatic growth conditions in the opportunistic yeast Candida albicans, but surprisingly only few of these overlapped with size control genes in the budding yeast Saccharomyces cerevisiae Here, we investigated one of the divergent potent size regulators in C. albicans, the Myb-like HTH transcription factor Dot6. Our data demonstrated that Dot6 is a negative regulator of Start, and also acts as a transcriptional activator of ribosome biogenesis (Ribi) genes. Genetic epistasis uncovered that Dot6 interacted with the master transcriptional regulator of the G1 machinery, SBF complex, but not with the Ribi and cell size regulators Sch9, Sfp1, and p38/Hog1. Dot6 was required for carbon-source modulation of cell size, and it is regulated at the level of nuclear localization by the TOR pathway. Our findings support a model where Dot6 acts as a hub that integrates growth cues directly via the TOR pathway to control the commitment to mitotic division at G1.

PMID: 30593490 [PubMed - indexed for MEDLINE]





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