Dataset Information

Tandem mass spectrometry of buffalo sperm-surface extracted proteins

ABSTRACT: The buffalo sperm surface proteins which are bound by either non-covalent (electrostatic)interactions or by a GPI-anchor were extracted and subjected to LC-MS/MS. The results revealed that proteins involved in the immune response and reproductive processes adorn the buffalo sperm surface.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Bubalus Bubalis Bubalis

TISSUE(S): Sperm

SUBMITTER: VIPUL BATRA

LAB HEAD: Tirtha Kumar Datta

PROVIDER: PXD022114 | Pride | 2021-08-13

REPOSITORIES: Pride

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Publications

Buffalo sperm surface proteome profiling reveals an intricate relationship between innate immunity and reproduction.

Batra Vipul V Bhushan Vanya V Ali Syed Azmal SA Sarwalia Parul P Pal Ankit A Karanwal Seema S Solanki Subhash S Kumaresan Arumugam A Kumar Rakesh R Datta Tirtha Kumar TK

BMC genomics 20210626 1

<h4>Background</h4>Low conception rate (CR) despite insemination with morphologically normal spermatozoa is a common reproductive restraint that limits buffalo productivity. This accounts for a significant loss to the farmers and the dairy industry, especially in agriculture-based economies. The immune-related proteins on the sperm surface are known to regulate fertility by assisting the spermatozoa in their survival and performance in the female reproductive tract (FRT). Regardless of their imp ...[more]

PMID: 34174811

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Project description:Somatic mutation in the X-linked phosphatidylinositol glycan class A (PIG-A) gene causes glycosylphosphatidylinositol (GPI) anchor deficiency in humans with Paroxysmal Nocturnal Hemoglobinuria (PNH). Clinically, patients with PNH have intravascular hemolysis, venous thrombosis and bone marrow failure. We produced a conditional Pig-a knock-out mouse model specifically inactivating the Pig-a gene in hematopoietic cells to study the role of PIG-A deficiency in PNH pathophysiology. We used Affymetrix Mouse Genome 430 2.0 chips to investigate the gene expression pattern in the mouse model of targeted Pig-a deletion. Experiment Overall Design: We performed microarray analysis on 3 pools of sorted GPI-deficient (GPI-) and GPI normal (GPI+) bone marrow cells derived from the same Pig-a knock-out animals, and identified 1275/669 genes of the 45,101 transcripts potentially available for screening using 2-fold change, <10% false discovery rate (FDR) and percentage of present calls as selection criteria. The major representative genes belong to the category of immune response. We tested whether the molecular differences between GPI- and GPI+ bone marrow cells could be preserved when GPI- cells were transplanted in lethally-irradiated wild type mice (C57BL/6). Microarray analysis was performed using sorted bone marrow cells from 4 animals transplanted with GPI-deficient bone marrow cells (T-GPI-) from Pig-a knock-out donors, 3 animals transplanted with GPI-normal bone marrow cells from C57BL/6 donors (T-GPI+), and GPI-normal bone marrow cells from 4 wild-type C57BL/6 mice (WT-GPI+). We found 296 probesets with 2-fold change cutoff, of which T-GPI- cells had 145 up-regulated genes in comparison to WT-GPI+ cells, and had 123 genes differentially expressed when compared to T-GPI+ cells. The gene expression of the GPI-deficient cells was very similar between the two sets of microarray experiments affirming the maintenance of the phenotype before and after bone marrow cell transplantation.

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