Dalya Antoun Gereige

Assistant professor
Life & Earth Sciences department - Section III - Tripoli
Speciality: Biology
Specific Speciality: Aspect moléculaires et cellulaires de la biologie

2014 - present : Assistant professor

Lebanese university - Faculty of sciences 3
Tripoli- lebanon

2013 - 2014 : Instructor

Lebanese university - Faculty of sciences 3
Tripoli- lebanon

2012 - 2012 : Post-doctoral fellow

Colmar France

Teaching 7 Taught Courses
(2014-2015) BioV 414 - Hormonal regulation and development genetic of plants

M1 Environmental and life Sciences - Option : Vegetal

(2014-2015) BIOV 415 - Hormonal regulation and development genetic of plants Lab

M1 Plant Biology and Environment

(2014-2015) Biol 114 - Organization of the plant living world and environment

BS Earth and life sciences

(2014-2015) Biol 114 - Organization of the plant living world and environment

BS Earth and life sciences

(2014-2015) BIOV 440 - Plant Biotechnology

M1 Plant Biology and Environment

(2014-2015) BIOV 441 - Plant Biotechnology Lab

M1 Plant Biology and Environment

(2014-2015) Biol 340 - Vegetal Physiology Lab

BS Earth and life sciences

2008 - 2012: PhD

Universite de strasbourg
Molecular and cellular biology

2006 - 2008: Masters

Universite Paris VI
Molecular and cellular biology

2003 - 2006:

Universite Saint Joseph
Life sciences

Conferences 1 participation
Publications 2 publications
Annette Niehl, Khalid Amari, Dalya Gereige2, Katrin Brandner, Yves Mély and Manfred Heinlein* Control of Tobacco Mosaic Virus Movement Protein Fate by CELL-DIVISION-CYCLE Protein 48 (CDC48). 2012

Like many other viruses, Tobacco mosaic virus replicates in association with the endoplasmic reticulum (ER) and exploits this membrane network for intercellular spread through plasmodesmata (PD), a process depending on virus-encoded movement protein (MP). The movement process involves interactions of MP with the ER and the cytoskeleton as well as its targeting to PD. Later in the infection cycle, the MP further accumulates and localizes to ER-associated inclusions, the viral factories, and along microtubules before it is finally degraded. Although these patterns of MP accumulation have been described in great detail, the underlying mechanisms that control MP fate and function during infection are not known. Here, we identify CELL-DIVISION-CYCLE protein48 (CDC48), a conserved chaperone controlling protein fate in yeast (Saccharomyces cerevisiae) and animal cells by extracting protein substrates from membranes or complexes, as a cellular factor regulating MP accumulation patterns in plant cells. We demonstrate that Arabidopsis (Arabidopsis thaliana) CDC48 is induced upon infection, interacts with MP in ER inclusions dependent on the MP N terminus, and promotes degradation of the protein. We further provide evidence that CDC48 extracts MP from ER inclusions to the cytosol, where it subsequently accumulates on and stabilizes microtubules. We show that virus movement is impaired upon overexpression of CDC48, suggesting that CDC48 further functions in controlling virus movement by removal of MP from the ER transport pathway and by promoting interference of MP with microtubule dynamics. CDC48 acts also in response to other proteins expressed in the ER, thus suggesting a general role of CDC48 in ER membrane maintenance upon ER stress.

Hu Q, Hollunder J, Niehl A, Kørner CJ, Gereige D, Windels D, Arnold A, Kuiper M, Vazquez F, Pooggin M, Heinlein M. Specific impact of tobamovirus infection on the Arabidopsis small RNA profile. 2011

Tobamoviruses encode a silencing suppressor that binds small RNA (sRNA) duplexes in vitro and supposedly in vivo to counteract antiviral silencing. Here, we used sRNA deep-sequencing combined with transcriptome profiling to determine the global impact of tobamovirus infection on Arabidopsis sRNAs and their mRNA targets. We found that infection of Arabidopsis plants with Oilseed rape mosaic tobamovirus causes a global size-specific enrichment of miRNAs, ta-siRNAs, and other phased siRNAs. The observed patterns of sRNA enrichment suggest that in addition to a role of the viral silencing suppressor, the stabilization of sRNAs might also occur through association with unknown host effector complexes induced upon infection. Indeed, sRNA enrichment concerns primarily 21-nucleotide RNAs with a 5′-terminal guanine. Interestingly, ORMV infection also leads to accumulation of novel miRNA-like sRNAs from miRNA precursors. Thus, in addition to canonical miRNAs and miRNA*s, miRNA precursors can encode additional sRNAs that may be functional under specific conditions like pathogen infection. Virus-induced sRNA enrichment does not correlate with defects in miRNA-dependent ta-siRNA biogenesis nor with global changes in the levels of mRNA and ta-siRNA targets suggesting that the enriched sRNAs may not be able to significantly contribute to the normal activity of pre-loaded RISC complexes. We conclude that tobamovirus infection induces the stabilization of a specific sRNA pool by yet unknown effector complexes. These complexes may sequester viral and host sRNAs to engage them in yet unknown mechanisms involved in plant:virus interactions.


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