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Candida albicans,  a common fungal pathogen which diverged from the baker’s yeast  Saccharomyces cerevisiae  has the unique ability to utilise N-acetylglucosamine, an amino sugar and exhibits phenotypic differences. It has acquired intricate regulatory mechanisms at different levels in accordance with its life style. N-acetylglucosamine kinase, a component of the N-acetylglucosamine catabolic cascade is an understudied gene since  Saccharomyces cerevisiae  lacks it. We report  HXK1  to act as both positive and negative regulator of transcription of genes involved in maintaining cellular homeostasis. It is involved in repression of hyphal specific genes in addition to metabolic genes. Its regulation of filamentation and GlcNAc metabolism is independent of the known classical regulators like  EFG1 ,  CPH1 ,  RAS1 ,  TPK2  or  TUP1 . Moreover, Hxk1-GFP is localised to cytoplasm, nucleus and mitochondria in a condition specific manner. By employing two-step affinity purification, we report the interaction of  HXK1  with  SIR2  under filamentation inducing conditions. Our work highlights a novel regulatory mechanism involved in filamentation repression and attempts to decipher the GlcNAc catabolic regulatory cascade in eukaryotes.

N-Acetylglucosamine Kinase, HXK1 Is Involved in Morphogenetic Transition and Metabolic Gene Expression in Candida albicans